Levodopa effects are more complex than said and not linked only to the sole dopaminergic neurons of substantia nigra.
Movement is a whole, resulting from many modulations that combinate to make it the appropriate one.
We have been all conditioned on one side by adepts of best science and on the other side, by big pharmas and key opinion leaders not to see
what any one knows when not polluted by the everyday flood of informations : We are not rats, even if we are treated as so
To move requires motor command, yes, but too, sensory inputs, cognitive functions, mood, motivation, desire, impulse, stress regulation, arousal,
attention, alertness, muscles, glucosis regulation.. all functions being directly or indirectly, fully or partially regulated by dopamine
and norepinephrin, molecules levodopa is the precursor of.
We have all misinterpretated for years, as conditioned to a simplificating thinking said to be the basic cause and effect relation for scientific demonstration.
Reality of complexity in effects and their regulations originate every question asked upon this forum.
Mucuna Pruriens is a plant, and again a far more complex substance than single levodopa
Mucuna has different properties explaining it works on PD, not only because of its Levodopa.
The ones that have ordered the trial in PD and afterwards patented Mucuna Pruriens are not stupid ones
The biggest problem is to modulate effects of treatments and here lays initially the superiority of plants with different molecules working
at different levels and characterized then with a kind of “adaptative possibility included”.
See the plants called “the adaptagenes” for stress.
In another thread you talk about the blocking inflammation and reactions to stress.
In fact, to follow this almost pradical way would lead us to hell when inflammation, here activation of microglia, is number one reaction to protect neurons.
And what would we do without stress response and no adaptation to continuous flow of hits and cascades of events?
I have neither the possibility* to give all the informations I learnt from my works, ,
a huge travel across all barriers too, nor to explain how all of them but I paste here a very short summary of the first page
of one important chapter about PD as seen through the INE network, written two years ago, some pages are yours too, Rick
No phenomena concerning neuronal networks in brain other may be understood as isolated of the framework of a whole entity, made of interacting complex sytems and ruled by biophysical laws.
Thus, the neuro-endocrine system and the immune system are linked together in a common network of interactions where immune cells express receptors for hormones, neurotransmitters, neuropeptides and respond to these agents and conversely, the immune system can send messages to the brain and neuro-endocrine associated structures that recognize and respond to these messengers.
Altogether compose a network of complex interactions that have immunoregulatory implications and that can also influence the activity of neuro-endocrine systems.
Furthermore, there is evidence that activated T cells can cross the blood-brain barrier and migrate into the CNS and may establish local immune-neuro-endocrine interactions in the CNS through the local release of cytokines that can affect the activity of neural cells.
As any other component of this immune-neuro-endocrine (INE) network, all the neural systems implicated in IPD are submitted to immune and endocrine influences and are related to brain interactions with the external environment and to stress regulation of the inner world through the HPA axis and the adrenergic sympathetic nervous system (SNS).
When exposure to environmental agents disrupt their coordinated adaptive responses, immune, hormonal and neural factors altogether contribute to determine whether recovery occurs quickly or does not happen.
Remember you get better results, longer ones though you take much less quantity of Levodopa from Mucuna P
than from tablets of synthetized Levodopa.
Concerning less side effects , not much may be concluded as the quantity is inferior .
For the good effects, more has to be said.
1. Mucuna has no dopadecarboxylase inhibitor ( no benserazide , no carbidopa) to shield it from your body's enzymes.
According to conventional wisdom, almost none should get to the brain. BUT it does.
Studies refute the presence of a peripheral decarboxylase inhibitor found in raw or boiled beans
2. Tryptamine alkaloids have been found in trace amounts (5-methoxy-NN, Dimethyltryptamine, also 5-hydroxy-tryptamine. )
3. Mucuna pruriens shows antioxidant and metal chelating activity
Volume 22 Issue 1, Pages 6 – 11 Published Online: 7 Dec 2007
Antiparkinson drug - Mucuna pruriens shows antioxidant and metal chelating activity
Muralikrishnan Dhanasekaran 1, Binu Tharakan 2, Bala V. Manyam 2 3 *
Parkinson's disease is a neurodegenerative disorder for which no neurorestorative therapeutic treatment is currently available.
Oxidative stress plays an important role in the pathophysiology of Parkinson's disease.
The ancient Indian medical system, Ayurveda, traditionally uses Mucuna pruriens to treat Parkinson's disease.
In our earlier studies, Mucuna pruriens has been shown to possess antiparkinson and neuroprotective effects in animal models
of Parkinson's disease.
The antioxidant activity of Mucuna pruriens was demonstrated by its ability to scavenge DPPH radicals,
ABTS radicals and reactive oxygen species. Mucuna pruriens significantly inhibited the oxidation of lipids and deoxyribose sugar.
Mucuna pruriens exhibited divalent iron chelating activity and did not show any genotoxic/mutagenic effect on the plasmid DNA.
These results suggest that the neuroprotective and neurorestorative effect of Mucuna pruriens may be related to its antioxidant activity independent of the symptomatic effect.
In addition, the drug appears to be therapeutically safe in the treatment of patients with Parkinson's disease.
4. Low dosages of levodopa enhance Growth Hormone release.
Mucuna requires much less levodopa to afford well being, why? Hard to say it simply.
• It’s a good point first because low dosages of levodopa permits to avoid or lessen the risks of side effects and complications
of immediate effects –hers,called adverse but demonstrated elsewhere– and also, a too important discontinuity in dopaminergic stimulation, when
pulsatile stimulation as it impairs functions. Both conditions, high dosage and correlated high pulsatility, known to be the main causes of motor complications, participate, at least partially, in the underlying process, the CNS impairements, leading to non motor -psychic and mental –complications.of levodopa
• Second point, low dosages of levodopa enhance Growth Hormone release.
Here is more, I would say much more, to be understood at different levels and in the INE networks.
This action is enhanced by amantadine but inhibited by vit B6 as it triggers peripheral accleration of the conversion of L- dopa to dopamine
Read this page below and you will see how complex effects are, to understand and to take in account.
• Second point, low dosages of levodopa enhance Growth Hormone release.
“I discovered that a major pharmaceutical company was using a local botanical product in the development of a prescription secretagogue
(= a substance which causes another substance to be secreted ).
This is not unusual as a large portion of prescription drugs are derived from plant sources by first isolating one active ingredient, denaturing it with a chemical side chain in order to patent it, then performing extensive clinical studies and finally submitting it, 21 million dollars later, to the FDA for approval. Upon examination, I found that the "active" ingredient was enhanced by the plant's other components.
Further, we found that a large amount of the activity of this ingredient was lost very rapidly (within 2 hours) after harvesting.
One of the active ingredients in this plant is L-dopa, a potent stimulator of GH release. I had worked extensively with L-dopa in the past as a consultant on its delivery.
L-dopa, used as an anti-aging drug and treatment for Parkinson's disease, is poorly absorbed and must be taken in super-physiologic doses (thousands of times what the body would produce in a day) in order to elicit a response.
At high doses, L-dopa can produce side effects, but at lower doses it will stimulate GH release, improve mental performance, and improve symptoms of Parkinson's disease
Growth hormone itself has produced improvements in Parkinson's disease; with the dual action of L-dopa and other secretagogues, and the lack of side effects, it's definitely worth a try for physician's to observe its -affect on patients who suffer from this devastating disease.
Studies conducted on the effectiveness of various amino acid stimulants of growth hormone release have produced significant results. One test for GH secretory potential is the arginine loading test, but very large amounts are used-often intravenously. Other amino acids like ornithine, lysine, and glutamine have produced mixed results
I had to ask myself, "How could the response to these amino acids vary to such a large extent?"
As it turns out, the study on L-glutamine that produced the most significant elevation in GH administered the amino acid in a carbonated drink solution. How could carbonation make that much of a difference in the effectiveness of this amino acid in GH release? I had tested effervescent delivery with L-dopa and other substances in the past and found it to be highly effective in combination with Chaperone Molecules. With carbonation, I had been able to produce rapid and efficient delivery of sensitive compounds. In this case, I discovered that effervescent delivery assists in the delivery of amino acids so that a greater and more consistent response can be derived with lower doses.
There are many receptors for these amino acids, so getting them to the right ones that stimulate GH release requires the use of Chaperone Molecules. In addition to protecting and delivering these amino acids, some Chaperone Molecules have insulin-regulating effects.
The importance of suppressing insulin in provoking GH release cannot be overstated. Blood sugar and insulin inhibit the release of growth hormone-this is a basic principle of the effectiveness of proper diet, fasting and exercise in stimulating GH. While consuming sugar and other carbohydrates in the diet will provoke insulin and inhibit GH release, there are other sugars, referred to as pharmaceutical saccharides that do not provoke insulin and are not metabolized as carbohydrates. In fact, when the right saccharides are used they do just the opposite-they help to regulate blood sugar and insulin. Some of these saccharides -like those in Symbiotropin- have a sweet taste, which eliminates the need for artificial or high carbohydrate sweeteners in flavoring the product.
I am not implying that insulin is the bad guy. In this highly complex system, we need insulin to promote the benefits of growth hormone. Studies show that GH fails to cause growth in animals lacking a pancreas and it also fails if carbohydrates (insulin provoking) are restricted from the diet. These studies reinforce our knowledge of insulin as a necessary catalyst in GH response and demonstrate that high levels of GH mean nothing in terms of results.
This is why I have concentrated on secretagogues, receptor site modulators, insulin regulation, and liver enzyme enhancers rather than GH injections.”
The pharmacologic effects of plant derived compounds are well documented in both human and animal clinical trials. These plant products possess structural similarities to endogenously produced hormones, which enhance their affinity to hormone receptors and steroid and prostaglandin dehydrogenases -making them effective adjuncts to a variety of hormone replacement therapies.
……..and so much more
These lines are written by pharmacologist James Jamieson who. knows perfectly well what he is talking about; no reference is given, but data are all evidence-based demonstrated –I have verified, as always, so do not mind the fact they are accompanying the sell of a product.
Link to James Jamieson explanations.
The worse about talking about Mucuna is that we ourselves may convince some to try, which may be good or bad, as we do not know all the conditions for it to work at best (there is no miraculous molecule in it! ) and that we only “work” for the incomes of money of some few we particularly disapprove.
But this has to be discussed in another thread, no?