Diesel0022
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Brah, it's been proven. A high quality L-Dopa product is superior for PRL control when compared to Dopa/B6. This isn't opinion or anecdotal evidence anymore. Same reason clinical applications tell you not to dose B6 with L-Dopa...L-dopa + pyridoxal phosphate >>> dopamine + pyridoxal phosphate + CO2
So for dopamine biosynthesis from L-dopa, pyridoxal phosphate is essential.
I'm sure you're familiar with mr.cooper69 aka. Cyrus?
Alright, I am going to quote Cy word for word from the text messages
It started on here, he stated that he "preferred dopadex", when compared to L-Dopa/P5P together.
And straight from the text messages "Using l-dopa with p5p is not optimal"
I confirmed with him before I posted this to make sure it was ok
You should not administer B6 with L-Dopa if you want L-Dopa to take on its full effects.
L-Dopa converts to Dopamine. Dopamine cannot cross the blood brain barrier. If you arent increasing brain dopamine levels, how are you doing anything for hormone release?
So, you want the conversion of L-Dopa to Dopamine to occur in the brain, NOT outside of the brain. When you combine B6 with L-Dopa it does in fact enhance this conversion, but it makes more of it happen OUTSIDE of the brain, not inside. So B6 makes L-Dopa less effective for bodybuilding purposes.
Inhibition of l-Dopa-Induced Growth Hormone Stimulation by Pyridoxine and Chlorpromazine
Abstract
One gram of l-dopa was administered orally to 12 male control subjects and induced an increase of growth hormone (GH) secretion. The l-dopa-induced GH response was inhibited by an intravenous infusion of pyridoxine, but pyridoxine did not inhibit the GH response to hypoglycemia. Chlorpromazine also inhibited l-dopa-induced GH stimulation. Glucose concentrations were unaffected by l-dopa, chlorpromazine, and pyridoxine administration in these subjects. The mechanism of the suppressed l-dopa-induced GH response by pyridoxine appears to be mediated by peripheral acceleration of the conversion of l-dopa to dopamine, while that of chlorpromazine appears to be mediated through hypothalamic centers. Pyridoxine and chlorpromazine should be added to the list of other factors affecting the response to L-dopa-induced GH stimulation.
Failure of vitamin B6 to reverse the l-dopa effect in patients on a dopa decarboxylase inhibitor
Abstract
Seven patients with Parkinsonism previously on l-dopa were placed on a regimen of l-dopa and alpha methyl dopa hydrazine (a dopa decarboxylase inhibitor). Two of these patients had previously shown marked clinical deterioration of the l-dopa improvement when given pyridoxine. None of the seven patients receiving alpha methyl dopa hydrazine demonstrated any change in their condition when given pyridoxine. The failure of vitamin B6 to reverse the clinical effect of l-dopa in patients receiving both l-dopa and a peripheral dopa decarboxylase inhibitor suggests that reversal of the l-dopa effect induced by vitamin B6 is due to increasing the activity of the enzyme dopa decarboxylase outside the central nervous system.
ON THE MECHANISM OF THE NULLIFICATION OF CNS EFFECTS OF l-DOPA BY PYRIDOXINE IN PARKINSONIAN PATIENTS
Abstract
Administration of either Levodopa (l-DOPA) or pyridoxine increased the concentration of dopamine in the basal ganglia of rats. However, administration of pyridoxine to rats pretreated with l-DOPA for several days resulted in a reversal of the l-DOPA-induced elevation of dopamine. Pretreatment of rats with Ro 4-4602 (an inhibitor of peripheral aromatic amino acid decarboxylases) enhanced the l-DOPA-induced rise in the CNS level of dopamine. This effect was also reduced substantially after the administration of pyridoxine. We interpret these results to indicate that the antagonistic effect of pyridoxine on the beneficial effects of l-DOPA in the CNS is centrally mediated as a result of decreased formation of dopamine.
Now you're asking: If P5P crosses blood brain barrier and so does L-Dopa shouldn't it enhance dopamine formation on both sides?
Yes, but, it also increases Dopamine conversion OUTSIDE the BBB by a much larger amount (more blood outside the brain than inside) so the net effect is negative. That's why you want an L-Dopa source that includes a decarboxylase inhibitor. Bulk 1-Carboxy from USP has that, and is a much more concentrated source of L-Dopa than just straight Mucuna. Decarboxylase inhibitors prevent excess conversion within the body.
Now for the complications. (Aren't there always complications
in life?) The final reaction to the neurotransmitter in both the
case of dopamine and serotonin, is decarboxylation, and the same
enzyme (the aromatic L-amino acid decarboxylase) is involved in
both conversions. This decarboxylase enzyme is present in the
liver, and it acts in the case of L-DOPA to convert the compound
to dopamine before it can make it into the brain (and if this
happens, the L-DOPA is wasted). The decarboxylase enzyme uses B6
as a cofactor for this reaction, and for this reason a
Parkinson's disease patient taking L-DOPA cannot take more than
the RDA of B6, because doing so would act to neutralize
oral L-DOPA too quickly. These days, almost all Parkinson's
patients on L-DOPA take the drug in a combination with an
artificial decarboxylase inhibitor, called Carbidopa (the
combination is called Sinemet). But even with Carbidopa,
Parkinson's patients are advised not to exceed a daily dose of B6
of 25 mg, since more will overwhelm the Carbidopa effect, and
cause pharmacologic L-DOPA to be destroyed in the liver before it
can get into the brain.
