Hello everyone! This is my first post, so I wanted to quickly send a BIG THANK YOU to all of the regulars on this forum. My Mom has Parkinson's and I've been immersing myself with information about the condition. Reading your personal experiences has been the most valuable source of information!!

After reading quite a bit about PD, there seems to be credibility to the idea that it may not just be a lack of dopamine that results in PD, but also imbalances in other neurotransmitters like norepinephrine and maybe others. It also seems like it's possible that carbidopa, as a general decarboxylase agent, may also inhibit the synthesis of tryptophan to seratonin ... leading to or contributing to depression. My Mom, like many other PWP, also suffers from depression and is on an SSRI to increase seratonin levels ... again showing that more than just dopamine is in play in this complicated condition (whether it's directly or indirectly related to PD or carbidopa).

Being new to the PD world and coming from an engineering/troubleshooting background, I was surprised that my Mom's neuro made no effort to actually measure my Mom's neurotransmitter levels and has taken a very myopic view of just using sinemet to increase dopamine levels. There is no analysis to see what else may be off balance that is contributing to the root cause of her PD ... or off balance because of the sinemet/carbidopa.

All this is just background to my real question ...

Do any of you have experience with a treatment plan that includes getting periodic blood platelet measurements of your catecholemine levels? It seems like a good idea to get a measure on the various neurotransmitter levels and treat accordingly in an effort to bring a balance ... and to make sure that certain neurotransmitters are not being depleted by her current therapy (e.g., carbidopa) over time. One example could be that if we find that her norepinephrine levels are low, maybe an antidepressive medication that works on both serotonin and norepinephrine may be a better option verus an SSRI. Another example could be that if we try a more natural approach like l-tyrosine or mucuna instead of sinemet, how does that affect her neurotransmitter levels. If we have measurements over time (e.g, every 6 months), we can track changes and make adjustments as necessary.

Any thoughts, feedback, criticism, experience with this approach?

THANK YOU in advance!

Neurotransitter imbalance is responsible for many things, even suspected in ADHD: they just found that multiple sclerosis patients lack norepinephrine. PD patients lack norepinephrine at autopsy as well as dopamine. Our adetylcholine is high when our dopamine is low. IMO it is acetylcholine and glutamate are all major players and highly toxic. Too much of them is why we overfire and we lack gabba. which is responaible for putting on the 'brakes". Serotonin is involed with mental functioning. Dopamine is a precursor to norepinephrine.

So you are on the mark at what you are reading. I have no clue why they do not test for them all. maybe the tests are new. Every pd patient should be tested for this before they start meds. And also for vitamin D.

You are astute and a fast learner. Be sure to let us know what you learn. That's how we do it, but reporting to each other . it is dangerous, for example to assume that a pwp can benefit from Alzheimers meds. especially the youger ones just to improve their memory or focus. THis results in a toxic build up that can paralyze a person.'

Here's a link and please add anything new you can find. I'm requesting to be tested for them at the end of this month - if you find anything else out please let me know.

Your mother is most fortunate to have a problem solver for a son.

http://www.integrativepsychiatry.net...ter_tests.html

sincerely

CarbiDOPA cannot cross the blood brain barrier

http://en.wikipedia.org/wiki/Carbidopa

it will be interesting to see where this is going.

One should test, of course. But few do.
At a minimum: the neurotransmitters, yes, but where? Dopamine in the gut - does it relate to the brain? what about ratios rather than absolute values? Does the level of "x" really matter so long as there is three times as much "y"? So, don't just run into the lab and throw money around. Think it through and have a reason for your decisions.

Don't stop with the brain neurotransmitters, though. In fact, don't even start with them unless you have the reasons. There are other tests that may be of more value to you. For example, There is ample reason to think that PD is driven by inflammation in the CNS. C-reactive protein gives info on the peripheral conditions, but what is going on past the blood brain barrier? Maybe you could learn more by tracking TNF-alpha or another cytokine. Keep in mind that these chemicals are neurotransmitters in their own right, too. We have had the opportunity to observe one of our number go down fast with an abscessed tooth from those chemicals and to bounce back as the antibiotics went to work.

Then there are the similar chemicals of the endocrine system's stress circuits. Cortisol is a reflection of chronic stress, but it is also a reflection of inflammation. Adrenaline is a marker of acute stress, but it can play hell with electrolytes, too. And don't forget the electrolytes! They are responsible for the functioning of both nerves and muscles. Yet, no one tests for them.

Look online and figure out how wide you can cast your net. Maybe you can find a sympathetic GP to give you a break on costs for drawing the specimens.

But share your data here. -Rick

Hi, it is good to have you here, and always nice to hear fresh voices and thinking.

AS I see it the problem with even trying to balance neurotransmitters is how do you know what 'normal' levels are in any given individual - they could vary considerably throughout the day, and are at work throughout the body not just the brain. Even taking sinemet is like taking a sledgehammer to a nut, as only a tiny amount gets to where it needs to go, it certainly does not target the SN directly. That is why taking it is a trail and error process, and you may have seen some of us use the analogy of 'walking a tightrope', when trying to manage our medications.

Having said that, and read Paula's post, in particular, there is something to be said for 'trying' to do something. Many of the neurotransmitters when out of balance give rise to other conditions, they are not the same as vitamins, and Paula has done a lot looking into this, and into which ones we may be lacking. An immediate one that some to mind is acetylcholine, as in terms of movement mechanics it provides the opposite message to dopamine. I take a medication in this class, for another PD related symptom, and it smooths my movement, and helps me not wear off. There are loads of them, and various non-neuro specialists who see PD patients for other things are aware from the anecdotal evidence of their patients that they can help with certain aspects of PD. As can some of the antidepressive medications.

Another problem with this is that neuros are and have been very l-dopa centric, but that is actually changing, and the wide range of studies being undertaken looking at this may eventually lead to treatments. But the passage of novel and good ideas through the pipeline to make it to patients is ver, very slow.

The better news is that some of these medications are actually licensed for other conditions.

Going back to my earlier point, trying to balance neurotransmitters still remains a trial and error thing, and other than l-dopa the best treatment that we know of is exercise, which can be very easy for some of us, and an immense hurdle for others. My guess is that when sufficiently exercised in a way that restores normal movement the body will generate some of the neurotransmitters and get them to the right places, and this will compensate for loss of dopamine, or trigger it's production in the non-SN areas of the brain and elsewhere in the body.

There is a great piece of video that was posted in recent weeks of a woman who is using chi kung, and nancyclist and many others are using exercise. How well this works in the very long term is something only time will tell.

I have strayed a little from the balance of neurotransmitters, but my personal belief is that the more naturally you can boost them or re-balance them the better, and it is likely that exercise will be found eventually to play a huge role in staving off the worst effects of PD.

Though how you get this to the people who are already far enough down the line to suffer from inertia and slowness is going to be an issue. Campaigning for care modalities that include exercise as a vital part of PD treatment is one possible way to go.

Lindy

i will discusss it with my neuro and with the NIH eval at the end if the month before I begin. I'm not that interested in dopamine - i want to know about actetycholine, glutamate, gaba, and norepinephrine. Without neuro and insurance help, it will be one at a time over a period of time if course - i think it's so relevant that i just have to do it.


paula

Paula, it would be great if it was established exactly what does go haywire when dopamine levels are reduced, and how the other NT's are affected, and what are the signs ........ then we might be able to see exactly what is happening in PD. But I do not see anyone doing this kind of thinking, or not in the scientific world anyway Every one is too busy looking at their own little bit of detail to look at a good overview of NT's ......... we must have all sorts of of compensatory things going on, thats how living things work, by making do with what they have got for as long as possible....

1: Am J Clin Nutr. 1984 May;39(5):722-9.

Diurnal variations in plasma concentrations of basic and neutral amino acids and
in red cell concentrations of aspartate and glutamate: effects of dietary protein
intake.

Maher TJ, Glaeser BS, Wurtman RJ.

The effects of dietary protein content on diurnal variations in plasma
concentrations of neutral and basic amino acids, and on red blood cell levels of
acidic amino acids, were studied in seven normal humans. The subjects consumed,
on three consecutive 3-day periods, diets containing 0, 75, or 150 g of egg
protein per day; blood was collected at 4-h intervals on the 2nd and 3rd days of
each diet. For each of the large neutral amino acids (LNAA; isoleucine, leucine,
tyrosine, phenylalanine, methionine, valine, and tryptophan) significant
correlations were observed between its plasma levels and the protein content of
the diet; highest levels were noted after consumption of the 150-g protein diet,
and lowest values after the O-g protein diet. For each LNAA, except tryptophan,
"fed" values (ie, those at 3 PM and 7 PM) were decreased relative to "fasting"
values (those at 3 AM and 7 AM) after consumption of the O-g protein-free diet,
but increased after consumption of the 150-g protein diet. Threonine, serine, and
proline behaved like the LNAA: in contrast, glycine and alanine rose after
protein-free meals and fell with the high-protein diet. The basic amino acids,
lysine, arginine, and histidine tended to respond like the LNAA to variations in
dietary protein content. Red blood cell concentrations of glutamate tended to
vary inversely with the protein content of the diet, while no relationship was
noted between red blood cell aspartate and dietary protein content. Food-induced
changes in plasma LNAA have been found to affect brain levels of amino acids that
are neurotransmitter precursors, as well as the syntheses of the transmitters
themselves.(ABSTRACT TRUNCATED AT 250 WORDS)


PMID: 6538743 [PubMed - indexed for MEDLINE]

Not terribly informative, but there is another post in the "traumatic brain injury" forum related to neuro testing ...

since i can't provide a link, if you are interested, please search for "neurotransmitter assessment and adrenal gland test" across all neurotalk forums

http://www.modernherbalist.com/Neurotest%20article.pdf




http://labdbs.com/

Treatment of Parkinson's Disease should not be with only levodopa. Parkinson's Disease treatment should be with properly balanced levodopa, 5-HTP, tyrosine, cysteine guided by neurotransmitter testing as indicted. Use of of this combination of nutrient controls the side effect of nausea associated with levodopa and prevents the depletion of serotonin and glutathione in treatment. It also helps prevent progression of Parkinson's Disease due to glutathione depletion which is needed


edited to add the controversial search results:

http://search.aol.com/aol/search?q=t...romesbox-en-us