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[LeonardElijah]

Do you take Adderall?

Buy a bottle of Methyl-B12.

The effects of Adderall slowly diminish over time. Prescriptions for Adderall to treat ADHD may, for some individuals, increase over time to produce the same effect. For instance, after a number of years, the prescription for 20mg a day becomes 30mg or 40mg.

In my experience, Methyl-B12 makes the Adderall seem "fresh" again.

What's going on?

It seems like it deserves a word of warning because Adderall is amphetamine, and we're adding a nice little "meth" group to it.

Methyl-B12 is half the equation in converting homocystine to SAMe. The other half of the equation is methylfolate. I recommend Metafolin methylfolate.

I don't think this is adding "meth" to the Adderall because methylfolate did not make Adderall for my ADHD fresh again. Only the methyl-B12 did.

Check it out.

Report back.

I don't think ANY doctors prescribe methyl-B12 alongside Adderall yet. I could be mistaken.

I'm curious about the relevant pathways and mechanism of action.

[ta5]

It inhibits glutamate/NMDA toxicity.

' class='bbc_url' title='External link' rel='nofollow external'>http://pmid.us/15371742']
Neuroreport. 2004 Oct 5;15(14):2241-4.
Group B vitamins protect murine cerebellar granule cells from glutamate/NMDA toxicity.
Lin Y, Desbois A, Jiang S, Hou ST.

The role of B group vitamins in preventing neuronal death against excitotoxicity was investigated. Neuronal death of cultured mouse cerebellar granule neurons (CGNs) caused by glutamate (50 microM) or NMDA (200 microM) was delayed in CGNs that had been treated with riboflavin (B2), folic acid (B9) or cynocobalamin (B12) for 18 h. Such neuroprotection by B2, B9 and B12 was in a dose- and time-dependent manner. In contrast, application of thiamin (B1), nicotinamide (B3), d-pantothenic acid (B5), pyridoxine (B6) or carnitine (BT) did not ameliorate glutamate or NMDA-mediated excitotoxicity to CGCs. These results are the first indication that certain B group vitamins are not only required for the normal brain function, but can also play a protective role against excitotoxicity to the brain.
PMID: 15371742

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' class='bbc_url' title='External link' rel='nofollow external'>http://pmid.us/7901032']
Eur J Pharmacol. 1993 Sep 7;241(1):1-6.
Protective effects of a vitamin B12 analog, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons.
Akaike A, Tamura Y, Sato Y, Yokota T.


The effects of methylcobalamin, a vitamin B12 analog, on glutamate-induced neurotoxicity were examined using cultured rat cortical neurons. Cell viability was markedly reduced by a brief exposure to glutamate followed by incubation with glutamate-free medium for 1 h. Glutamate cytotoxicity was prevented when the cultures were maintained in methylcobalamin-containing medium. Glutamate cytotoxicity was also prevented by chronic exposure to S-adenosylmethionine, which is formed in the metabolic pathway of methylcobalamin. Chronic exposure to methylcobalamin and S-adenosylmethionine also inhibited the cytotoxicity induced by N-methyl-D-aspartate or sodium nitroprusside that releases nitric oxide. In cultures maintained in a standard medium, glutamate cytotoxicity was not affected by adding methylcobalamin to the glutamate-containing medium. In contrast, acute exposure to MK-801, a NMDA receptor antagonist, prevented glutamate cytotoxicity. These results indicate that chronic exposure to methylcobalamin protects cortical neurons against NMDA receptor-mediated glutamate cytotoxicity.
PMID: 7901032

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