Swept,

Do you have type O blood?I do and also find protein is synergistic with sinemet.

md[/QUOTE]

No Im A positive but intresting point is blood group a predictor must be data out there somewhere over the rainbow

Once upon a time this group was incarnated as "Brain Talk" until things got weird there and the refugees settled here. But at some point prior to that diaspora, we had an extensive discussion about this very subject. As I recall, about half of us were Type O and did indeed thrive on protein.

No Im A positive but intresting point is blood group a predictor must be data out there somewhere over the rainbow[/QUOTE]

[/QUOTE]

What I was thinking but didnt elaborate was that there is an incredible pool of observational information here that is wasted,but if we throw it all in a blender,what would we get a profile of a PWP,a bit simplistic,I know,just a thought seed.

I feel that your inspiring story cannot be explained by revival of the dopamine producing cells but rather it indicates a flow in the the theory that PD is only a "dopamin loss" illness. I am no scientist but can any body explain to me the following simple questions:
- Why Ldopa is ineffective to treat the major PD symtom which is tremor in about 50% or more patients?
- Why Ldopa stops to be useful after one to 5 years?
- Why Ldopa causes diskinesia and on/off symptom eventually?

Wishing you best health
Imad

Hi Imad,
First of all, I don't think the questions are all based on correct data.
Levodopa is used to reduce tremor, I know various PD sufferers who only have a tremor as their main or only symptom who take levodopa to reduce or eliminate it. See http://www.guide4living.com/parkinsons/tremors.htm

Treatment for Parkinson’s Tremors
Early tremors are sometimes treated with anticholinergic drugs which work to restore the balance of the neurotransmitters dopamine and acetylcholine – the former is deficient in Parkinson’s patients whereas the latter is often overactive. However levadopa-based drugs such as Madapor and Sinemet are becoming the mainstay of treatment and have been found to be fast-acting in controlling.

Your second question, " Ldopa stops to be useful after one to 5 years?"
is also not right. I am approaching 20 years with PD, and I get relief for all my symtoms with Levodopa even at low dose. Problem is PWP are not all alike. You could probably find an example where it has become inactive after 5 years.

Your 3rd question, "Why Ldopa causes diskinesia and on/off symptom eventually?".
I would love to know why dyskinesia occurs. It is certainly caused by levodopa, as well as other things, but why no-one knows All I can say is levodopa does cause dyskinesia and in my case it started about year 8 or 9.
Amantadine is prescribed for some relief, but it becomes ineffective after 6 to 9 months.

Sorry to sound so negative, but I believe the above is correct, hope it helps.
Ron

Hi Imark,
This is pretty cheeky of me to respond after Ron has made excellent points to your questions. You sound discouraged - L-dopa not working for you?
L-dopa works well for tremor for many people for many years - not just up to 6 years. I have been taking it for 13 years (1-3 doses/day 25/100) and works well for me and no dyskinesia. Have you considered DBS? which is teriffic for reducing or getting rid of tremor, allows you to cut down on your medication thus stops the dyskinesia. Dyskinesia occurs as your disease progresses requiring you to take more and more L-Dopa (Dopa does not stop working, you just need a lot more to control your symptoms untill you reach a point where the side effect - dyskinesia is worse than the disease itself. For unknown reasons, the brain becomes hypersensitive to all the dopamine being thrown at it.

I do not have tremor nor dyskinesia (20 years) but as Ron said, all PWP are not created equal.

TG

Thank you Ron for your reply and you know that I hold your opinions in very high esteem.

With regard my statement that sinemet benefiting only 50% of PD patients is based on what I was told by more than one neurologist. They told me “if sinemet helps with tremor, this is a bonus”. I recall reading posts on this forum stating that sinemet did not help with their tremor. I think it is a valid question: why Ldopa does not help a considerable ratio of WPD’s in the most common symptom of PD, if PD is a “dopamin insufficiency” disease.

With regard the second point, we are all familiar with the commonly phrased expression: the sinemet honeymoon, which lasts from 1 to 5 years.

As with last point, is it not valid to question the “dogma” that dopamine insufficiency is the only cause of PD, after 50 years of using Ldopa with millions of patients, we still don’t know the answer to fundamental questions about it such why it causes diskinesia and on/off symptoms.

Imad

Its still a great mystery,the book Quia Imperfectum charts the research men responsible for the beginings of treatment with levadopa drug therapy for PD and the story continues.
L-DOPA, is still misunderstood in terms of its neurotoxic potential and its mechanisms

Below a few abstracts of many on current avenues of investigation and discovery


The undesired motor dyskinesias that commonly accompany long-term L: -DOPA therapy, can be viewed as
an outcome of L: -DOPA's sensitizing DA receptors (D(1)-D(5)), The newest findings
demonstrate that L: -DOPA induces BDNF release from corticostriatal fibers, which
in-turn enhances the expression of D(3) receptors; and that this effect is
associated with motor dyskinesias (and it is blocked by D(3) antagonists). The
recent evidence on mechanisms and effects of L: -DOPA increases understanding
of thiedrug, and can lead to improvements in L:-DOPA effects while providing avenues for reducing or eliminating L: -DOPA's
deleterious effects.
------------------------------------------------------------------------------------------------------------
Pulsatile activation of type D2 dopamine
receptors is reported to be the principal factor in the triggering of dyskinesias
and may well be involved in the priming phenomenon. While the pathophysiological
basis of priming is not yet known, the phenomenon would not appear to be related
to a hyperexpression of dopamine receptors (types D1 and D2) in the sensorimotor striatum. The results of recent experiments have given rise to several different hypothesis for the mechanisms involved in priming: the role of internalization of dopamine receptors after administration of dopaminergic drugs; change in the distribution of D3 dopamine receptor; changes in the expression of peptides (substance P, enkephalin) in efferent neurons of the striatum; and reorganization of connections at the level of the dopaminergic neurons and their target tissue.
While many questions remain unanswered, it may well be that the initial
therapeutic decisions taken when treating de novo patient are crucial in trying
to delay the onset of dyskinesias


Quote from the book Qiua Imperfetum
If you use it right following the methods I have worked out the effects last a lifetime. WHAT DID HE MEAN


In 1977, George Cotzias, et al. reported a 50% increase in the mean lifespan of rats fed very high doses of L-Dopa, the precursor to the neurotransmitter dopamine. In another study in rats, it was shown that the incidence of movement disorders among aged rats were almost totally reversed by L-Dopa, which enabled the rats to swim almost as well as young rats. L-Dopa is used to treat Parkinson's disease patients, with major improvements usually occurring for several years followed by a steep decline in function coupled with adverse side effects. The problem with L-Dopa as an antiaging drug is its side effects at high doses, which include abnormal heart rhythms, movement disorders, mental disturbances, and a greater risk of at least one type of cancer.


Hmmmm questions questions