It's no secret that Mucuna is extracted and utilized for its high content of natural L-DOPA martin, you've levied no revelations there. What may be a revelation to you, however, is Mucuna's propensity to carry natural decarboxylase inhibitors such as carbidopa, making it vastly more effective than its synthetic counterpart. What may be a revelation to you as well, is the expression of COQ-10 and complex-I which have neurorestorative effects on the dopaminergic ions in the substantia nigra. What may be a revelation, is that unlike the synthetic L-DOPA you speak of, MP actually regenerates endogenous levadopa, dopamine, norepinephrine and GH levels. I think it seems rather redundant here to mention that it actually increases hypothalamatic-pituitary-axis GH production by way of raising (and keeping high) levels of GHRH.
Posting a title like this is quite similar to "Designer Supplements..full of ****?" then imparting the board with your knowledge that DS extracts 3-4 divan., from the Nettle Root.
So, your question of "is this little more than L-DOPA?" seems rather juvenile in the proper context. What was it, exactly, that you assumed Mucuna was extracted for? It's sweet aroma, therein raising serotonin levels to produce a euphoric effect?
As you seem to lack the motivation to do some necessary research before you attack a product, let me hit you with a little knowledge son:
Mucuna pruriens in Parkinson's disease: a double blind clinical and pharmacological study.
* Katzenschlager R,
* Evans A,
* Manson A,
* Patsalos PN,
* Ratnaraj N,
* Watt H,
* Timmermann L,
* Van der Giessen R,
* Lees AJ.
National Hospital for Neurology and Neurosurgery, London, UK.
BACKGROUND: The seed powder of the leguminous plant, Mucuna pruriens has long been used in traditional Ayurvedic Indian medicine for diseases including parkinsonism. We have assessed the clinical effects and levodopa (L-dopa) pharmacokinetics following two different doses of mucuna preparation and compared them with standard L-dopa/carbidopa (LD/CD). METHODS: Eight Parkinson's disease patients with a short duration L-dopa response and on period dyskinesias completed a randomised, controlled, double blind crossover trial. Patients were challenged with single doses of 200/50 mg LD/CD, and 15 and 30 g of mucuna preparation in randomised order at weekly intervals. L-dopa pharmacokinetics were determined, and Unified Parkinson's Disease Rating Scale and tapping speed were obtained at baseline and repeatedly during the 4 h following drug ingestion. Dyskinesias were assessed using modified AIMS and Goetz scales. RESULTS: Compared with standard LD/CD, the 30 g mucuna preparation led to a considerably faster onset of effect (34.6 v 68.5 min; p = 0.021), reflected in shorter latencies to peak L-dopa plasma concentrations. Mean on time was 21.9% (37 min) longer with 30 g mucuna than with LD/CD (p = 0.021); peak L-dopa plasma concentrations were 110% higher and the area under the plasma concentration v time curve (area under curve) was 165.3% larger (p = 0.012). No significant differences in dyskinesias or tolerability occurred. CONCLUSIONS: The rapid onset of action and longer on time without concomitant increase in dyskinesias on mucuna seed powder formulation suggest that this natural source of L-dopa might possess advantages over conventional L-dopa preparations in the long term management of PD. Assessment of long term efficacy and tolerability in a randomised, controlled study is warranted.
