Hi,
I'm 46 and have been diagnosed with PD 9 months ago (confirmed by DatScan). I'm taking Azilect but not taking L-Dopa yet (I'm also taking Vit E and CoQ10 - but this was "self-prescribed" as I understand they are good anti-oxidants and don't seem to have much drawbacks - hope it's true).
I'm not a medical doctor but been reading a lot about the medical aspects of it and am trying to find out the "root cause" of PD for me (I suspect different people will get PD because of different causes). If anyone tried something similar - or just wish to comment or provide ideas - I would welcome your feedback.
Here's a quick summary of my approach and my understanding so far (again: note that I'm not a medical doctor, so this could be all wrong):
My understanding is that PD arrives when (a) our brain produces too little dopamine or (b) too many dopaminic neurons get destroyed.
At least for the first (too little dopamine), there seems to exist a "formula" of how the brain normally creates dopamine. To me this formula implies that in order to create dopamine at "normal" levels the brain needs to have a "normal" supply of all the key "ingredients" in the formula, which are: (1) L-Dopa, (2) something called "Pyridoxal-phosphate" (which essentially seems to be vitamin B6), and (3) something else with another great name ("Aromatic L-amino acid decarboxylase"). My understanding is that one needs to have the right balace of these 3 ingredients for things to work well (and please note that I keep reading that too much of one "ingredient" alone can also be harmful.. so pls don't start taking vit B6 complements on a "just-in-case" basis after you read this as I have no clue, but it could just make things worse if you already have too much of it).
Also, for the brain to create L-Dopa on its own, there is another formula that explains the key "ingredients". These seem to mainly include vit B9, Iron, Oxygen, and 3 other things with those great long names that nobody can read.
Trying to figure out what causes neuron destruction (my point "b" above) is more difficult to me. So far, the main point I found is that deficiency in vit B9 also seems to create cell oxidation which means it destroys the neurons (thus making vit B9 deficiency double negative - not only it prevents your brain from creating L-Dopa naturally, but it also destroys the neurons that create dopamine).
The good news is that it seems doable (and even easy) to test what is the current level that one has of many of the "ingredients" I mentioned above. Blood tests seem to exist for Iron, Vitamin B6, Vitamin B9, Oxygen concentration, for L-Dopa levels, and for several of the other long-named-ingredients. Obviously blood tests check the levels of these things in the blood (and not in the brain), but I'm presuming that if there's not enough of something in my blood, then my brain is not going to make it out of thin air anyway. A couple of the "ingredients" seem a bit more difficult to test... but most seem very doable.
My logic is that once I know which "ingredients" I'm low on, then I can try to look for what is the cause that explains why it's low and try to correct that (or if harmless and feasible, take complements of that). In my case, I already know that I'm low on Iron and suspect I may also be low on some of the B vitamins (and I further suspect that these come from gastric problems... which I had for many years). I also suspect I may have some oxygen-related problems (but these seem a lot more complex, so starting with the "easy" ones first).
The bad news is that I'm finding it hard to get a real medical doctor to help me do this (obviously, I can't do blood or other tests without a doctor prescription and my neurologist seems to find any investigations a waist of time). So, I'm advancing at snail pace. And I'm obviously not going to start taking vit B9 or B6 supplements "just-in-case" without a real medical doctor behind me to ensure I'm not messing up something else.
So, any suggestions, comments or feedback is welcomed,
Good luck to all,
lfs
I may be wrong but I believe that, at least for normal PD, the immediate cause is always the destruction of the cells in the substantia nigra and not your cause 1, Why these cells die is, as far as I know due to the aggregation of alpha-synuclein to make lewy bodies. But, as far as I know, no-one is sure why the alpha-synuclein does this though in the cases of familial parkinsons it is probably linked to gene mutations. External toxins, diseases, food etc have been linked but no firm causation has been proved.
I think we would all like to know what happened and why, but, except for the genetic family bunch (about 5% ?)I doubt we ever will. In the end it doesn't matter as it is stopping the continued process of destruction that counts, not what triggered it off. The arsonist is long gone, is putting out the fire that is urgent. Since the problem is at the micro-cellular level I don't thing any of us can be our own firemen, we just have to wait for the professionals.
though exercise, clean living, positive attitude etc etc probably help with the symptoms.
I think we would all like to know what happened and why, but, except for the genetic family bunch (about 5% ?)I doubt we ever will. In the end it doesn't matter as it is stopping the continued process of destruction that counts, not what triggered it off. The arsonist is long gone, is putting out the fire that is urgent. Since the problem is at the micro-cellular level I don't thing any of us can be our own firemen, we just have to wait for the professionals.
though exercise, clean living, positive attitude etc etc probably help with the symptoms.
Hi Turnip
Thanks for your response and maybe you’re totally right. I too, of course, look forward to the day where the professionals will figure out a way to deal with PD once and for all.
I also fully agree with you that the destruction of the cells in the substantia nigra may be the factor behind PD, but I’m a little surprised that you say it always is. Can you please explain why you say that?
Note that I’m a bit surprised because I understood that DaTscans only measured the activity of Dopamine Transporters – not whether the cells were dead or alive. Also, there seems to be plenty of reasonable evidence that folks with PD had a higher-than-average incidence of anemia and gastro-intestinal symptoms for many years before PD symptoms develop (and I did too)… which is consistent with the hypothesis that PD may develop because of long-term deficiencies in the ability to create dopamine (as anemia really means low oxygen in blood and is often also linked to iron deficiency; and gastro-intestinal symptoms can sometimes also be linked to mal-absorption problems). So my hypothesis is that if you have enough of these factors playing in the wrong way you may get PD as a consequence.
But, of course, this is just my hypothesis and even if it proves to be correct, you could still be totally right that once you get the symptoms it may just be too late already to do anything. But right now I believe there might be a chance (even if small) and while I believe in it I'll just keep looking until I exhaust all possibilities :-)
Warm regards and thanks for your thoughts,
lfs
Thanks for your response and maybe you’re totally right. I too, of course, look forward to the day where the professionals will figure out a way to deal with PD once and for all.
I also fully agree with you that the destruction of the cells in the substantia nigra may be the factor behind PD, but I’m a little surprised that you say it always is. Can you please explain why you say that?
Note that I’m a bit surprised because I understood that DaTscans only measured the activity of Dopamine Transporters – not whether the cells were dead or alive. Also, there seems to be plenty of reasonable evidence that folks with PD had a higher-than-average incidence of anemia and gastro-intestinal symptoms for many years before PD symptoms develop (and I did too)… which is consistent with the hypothesis that PD may develop because of long-term deficiencies in the ability to create dopamine (as anemia really means low oxygen in blood and is often also linked to iron deficiency; and gastro-intestinal symptoms can sometimes also be linked to mal-absorption problems). So my hypothesis is that if you have enough of these factors playing in the wrong way you may get PD as a consequence.
But, of course, this is just my hypothesis and even if it proves to be correct, you could still be totally right that once you get the symptoms it may just be too late already to do anything. But right now I believe there might be a chance (even if small) and while I believe in it I'll just keep looking until I exhaust all possibilities :-)
Warm regards and thanks for your thoughts,
lfs
do you take PPI for your gastric problems ? (Lanzaprole etc)
I discovered the other day that they may inhibit take up of B12 via food (but not supplements )
I've just added B12 to the long list of supplements I take
do your research carefully, and don't be afraid to experiment
I discovered the other day that they may inhibit take up of B12 via food (but not supplements )
I've just added B12 to the long list of supplements I take
do your research carefully, and don't be afraid to experiment
Hi Krugen68,
Thanks for your comments - appreciate it!
I'm not taking anything for my gastric problems at this moment. I'm doing some pretty comprehensive testing of my gastric system as 12 years ago I tested positive for a bacteria called helicobacter pylori (for which I took antibiotics at that time - apparently with good results as I tested negative for this bactery a month ago), my low iron levels could also be linked to gastric problems, and anyway I have some softer symptoms that I make me believe there's something in there. I have more gastric tests scheduled for a couple of weeks from now.
Interestingly, I read somewhere recently that helicobacter pylori actually reduces gastric acid and some of the typical symptoms of low gastric acid do seem to match my own symptoms... so gastric-acid wise, I'm actually more inclined to think that I have low level rather than high (actually symptoms of both low and high gastric acid are not that different in some aspects - so be carefull to check both if some of you are looking into this area). The other hypothesis I am considering is that intestinal flora composition may cause absorption problems. But measuring or changing intestinal flora composition doesn't seem to be that easy (though one easy think to do seems to be these activia/actimel youghourts - I was told by one gastro-enterologist that they can be pretty effective at promoting the growth of some beneficial bacteria).
Cheers,
lfs
Thanks for your comments - appreciate it!
I'm not taking anything for my gastric problems at this moment. I'm doing some pretty comprehensive testing of my gastric system as 12 years ago I tested positive for a bacteria called helicobacter pylori (for which I took antibiotics at that time - apparently with good results as I tested negative for this bactery a month ago), my low iron levels could also be linked to gastric problems, and anyway I have some softer symptoms that I make me believe there's something in there. I have more gastric tests scheduled for a couple of weeks from now.
Interestingly, I read somewhere recently that helicobacter pylori actually reduces gastric acid and some of the typical symptoms of low gastric acid do seem to match my own symptoms... so gastric-acid wise, I'm actually more inclined to think that I have low level rather than high (actually symptoms of both low and high gastric acid are not that different in some aspects - so be carefull to check both if some of you are looking into this area). The other hypothesis I am considering is that intestinal flora composition may cause absorption problems. But measuring or changing intestinal flora composition doesn't seem to be that easy (though one easy think to do seems to be these activia/actimel youghourts - I was told by one gastro-enterologist that they can be pretty effective at promoting the growth of some beneficial bacteria).
Cheers,
lfs
Hi lfs
not only did I catch shigella dysentery in West Africa years ago(in my 20s), I then had a duodenal ulcer 20 years later. I makes you wonder
H Pylori And Parkinson’s Disease – The Helicobacter Study
Just over a week ago, a group of researchers presenting at the 111th General Meeting for the American Society of Microbiology revealed their research looking into the relationship between the bacterium Helicobacter pylori and the development of Parkinson’s Disease, and their results were surprising to say the least.
Given that many readers of this site are interested in H pylori moreso than ulcers, I figured I would evaluate the study and what it means for the general population (after all, over half of the World’s population is thought to have an H pylori infection).
The researchers reported that both infecting mice with H pylori and feeding mice food contaminated with dead H pylori bacteria led to movement degeneration, typical of Parkinson’s Disease (1). Here is the overview of the results (note: all bullet points reference resource 1):
•1. Aged mice developed unusual and impaired movement. This signals low levels of dopamine, suggesting that dopamine-producing cells in the brain either died or were impaired. At a basic level, Parkinson’s Disease is the unexplained dying off of dopamine-producing cells.
•2. Young mice were largely unaffected by both the feedings and infection.
•3. Mice fed dead H pylori also developed symptoms.
•4. Different strains of H pylori produced different results. In particular, the “ΔAlpAB” strain seemed to cause more advanced degeneration and increased levels of inflammation.
Now the real question is, what do these results mean for the every day person? Below, we will investigate the four primary findings.
1. Aged mice developed unusual or impaired movement
After consuming H pylori or being infected, the aged mice developed movement deficits. The researchers in this case assumed that the the deficits were due to dopamine-producing cell death, just like in Parkinsons, but these results were not confirmed.
It is possible another mechanism contributed to these movement deficiencies. It also should be known that mice do not get Parkinson’s disease, and that the mice in the study simply developed symptoms similar to Parkinson’s disease.
This is not the first time this has been proposed before. In 1965, a researcher proposed that there was a link between stomach ulcers and Parkinson’s Disease, long before H pylori was brought to the attention of the mainstream medical community (2).
2. Young mice were largely uneffected by H pylori infection
In my opinion, this is one of the most interesting results of the study. This seems to verify one of the hypotheses of the researcher behind the African Enigma research paper.
If you are unfamiliar with this paper, the researcher reports that H pylori is very prevalent in Africa whereas ulcers, stomach ulcer symptoms, and other side effects are not very prevalent at all (3). One hypothesis he uses to explain this phenomenon was the notion that people who are infected with H pylori at a young age seem to not be as strongly affected as those who are infected as adults (3).
This mouse study seems to actually corroborate this nearly 20-year old hypothesis; young mice infected with H pylori did not develop symptoms, only old mice infected or fed H pylori developed motor impairments (1).
3. Mice fed dead H pylori bacteria also developed symptoms
The point of feeding mice dead H pylori was an attempt to verify the idea that it is not infection with H pylori itself that causes Parkinson’s Disease, but rather that H pylori produces a neurotoxic compound that might kill off nerve cells. Both dead and alive H pylori possess this compound.
This hypothesis stemmed from the discovery that high rates of Parkinson’s Disease in a certain native tribe were caused by a neurotoxic seed that made up a large part of their diet. The compound produced by H pylori is very similar to the neurotoxin found in the seed which is known to cause Parksinson’s.
This piece is perhaps the strongest bit of evidence presented by the researchers. The only downside of this portion is that mice were exposed to H pylori levels which are not likely to occur naturally; contaminated human food would never contain the same levels of bacteria that was given to the mice in the study.
4. Different strands of H pylori produced different results
This conclusion was also extremely interesting. Once again, the author of the The African Enigma research paper suggested that one reason for differences in response to H pylori on different continents might be due to different strains of H pylori.
The researchers used two different types of H pylori in their experiments, and found that one strain of H pylori in particular caused significantly more damage and inflammation than the “standard” strain of H pylori bacteria (1).
It is within the realm of possibility that certain strains of H pylori might result in different effects on the human body.
H Pylori and Parkinson’s Disease – Conclusion
While the initial evidence linking H pylori and Parkinson’s is strong and based on logical grounds, it is still too soon to take anything away immediately from this particular study, and this study raises at least as many questions as it answers.
The main problem is simple: why is H pylori so much more prevalent than Parkinson’s Disease? It could be for a variety of reasons, such as:
H pylori which does not infect its host until late adulthood may be more dangerous than H pylori present for a lifelong infection;
Different strains of H pylori may exist across regions and continents, making some infections more dangerous than others;
Areas of high H pylori infection rates also tend to lack sanitation and modern medical treatments, resulting in relatively lower life expectencies. It is possible that many people with H pylori just might not live long enough to get Parkinson’s Disease;
And finally, the results of this study may not actually carry over to humans.
The bottom line is that it is far too soon to tell whether or not H pylori contributes to Parkinson’s, and we will not know until more research has been performed.
If you are still concerned about the possible links, be sure to discuss this with your doctor. Perhaps there may be some merit to testing for H pylori in the absence of symptoms if you are an otherwise healthy adult with a family history of Parkinson’s Disease. However, that should be a discussion between you and your doctor.
References
1. M.F. Salvatore, S.L. Spann, D.J. Mcgee, O.A. Senkovich, & T.L. Testerman. Helicobacter pylori infection induces Parkinson’s Disease symptoms in aged mice. Presentation at the 111th General Meeting for the American Society for Microbiology. 2011 May 22. New Orleans, LA.
not only did I catch shigella dysentery in West Africa years ago(in my 20s), I then had a duodenal ulcer 20 years later. I makes you wonder
H Pylori And Parkinson’s Disease – The Helicobacter Study
Just over a week ago, a group of researchers presenting at the 111th General Meeting for the American Society of Microbiology revealed their research looking into the relationship between the bacterium Helicobacter pylori and the development of Parkinson’s Disease, and their results were surprising to say the least.
Given that many readers of this site are interested in H pylori moreso than ulcers, I figured I would evaluate the study and what it means for the general population (after all, over half of the World’s population is thought to have an H pylori infection).
The researchers reported that both infecting mice with H pylori and feeding mice food contaminated with dead H pylori bacteria led to movement degeneration, typical of Parkinson’s Disease (1). Here is the overview of the results (note: all bullet points reference resource 1):
•1. Aged mice developed unusual and impaired movement. This signals low levels of dopamine, suggesting that dopamine-producing cells in the brain either died or were impaired. At a basic level, Parkinson’s Disease is the unexplained dying off of dopamine-producing cells.
•2. Young mice were largely unaffected by both the feedings and infection.
•3. Mice fed dead H pylori also developed symptoms.
•4. Different strains of H pylori produced different results. In particular, the “ΔAlpAB” strain seemed to cause more advanced degeneration and increased levels of inflammation.
Now the real question is, what do these results mean for the every day person? Below, we will investigate the four primary findings.
1. Aged mice developed unusual or impaired movement
After consuming H pylori or being infected, the aged mice developed movement deficits. The researchers in this case assumed that the the deficits were due to dopamine-producing cell death, just like in Parkinsons, but these results were not confirmed.
It is possible another mechanism contributed to these movement deficiencies. It also should be known that mice do not get Parkinson’s disease, and that the mice in the study simply developed symptoms similar to Parkinson’s disease.
This is not the first time this has been proposed before. In 1965, a researcher proposed that there was a link between stomach ulcers and Parkinson’s Disease, long before H pylori was brought to the attention of the mainstream medical community (2).
2. Young mice were largely uneffected by H pylori infection
In my opinion, this is one of the most interesting results of the study. This seems to verify one of the hypotheses of the researcher behind the African Enigma research paper.
If you are unfamiliar with this paper, the researcher reports that H pylori is very prevalent in Africa whereas ulcers, stomach ulcer symptoms, and other side effects are not very prevalent at all (3). One hypothesis he uses to explain this phenomenon was the notion that people who are infected with H pylori at a young age seem to not be as strongly affected as those who are infected as adults (3).
This mouse study seems to actually corroborate this nearly 20-year old hypothesis; young mice infected with H pylori did not develop symptoms, only old mice infected or fed H pylori developed motor impairments (1).
3. Mice fed dead H pylori bacteria also developed symptoms
The point of feeding mice dead H pylori was an attempt to verify the idea that it is not infection with H pylori itself that causes Parkinson’s Disease, but rather that H pylori produces a neurotoxic compound that might kill off nerve cells. Both dead and alive H pylori possess this compound.
This hypothesis stemmed from the discovery that high rates of Parkinson’s Disease in a certain native tribe were caused by a neurotoxic seed that made up a large part of their diet. The compound produced by H pylori is very similar to the neurotoxin found in the seed which is known to cause Parksinson’s.
This piece is perhaps the strongest bit of evidence presented by the researchers. The only downside of this portion is that mice were exposed to H pylori levels which are not likely to occur naturally; contaminated human food would never contain the same levels of bacteria that was given to the mice in the study.
4. Different strands of H pylori produced different results
This conclusion was also extremely interesting. Once again, the author of the The African Enigma research paper suggested that one reason for differences in response to H pylori on different continents might be due to different strains of H pylori.
The researchers used two different types of H pylori in their experiments, and found that one strain of H pylori in particular caused significantly more damage and inflammation than the “standard” strain of H pylori bacteria (1).
It is within the realm of possibility that certain strains of H pylori might result in different effects on the human body.
H Pylori and Parkinson’s Disease – Conclusion
While the initial evidence linking H pylori and Parkinson’s is strong and based on logical grounds, it is still too soon to take anything away immediately from this particular study, and this study raises at least as many questions as it answers.
The main problem is simple: why is H pylori so much more prevalent than Parkinson’s Disease? It could be for a variety of reasons, such as:
H pylori which does not infect its host until late adulthood may be more dangerous than H pylori present for a lifelong infection;
Different strains of H pylori may exist across regions and continents, making some infections more dangerous than others;
Areas of high H pylori infection rates also tend to lack sanitation and modern medical treatments, resulting in relatively lower life expectencies. It is possible that many people with H pylori just might not live long enough to get Parkinson’s Disease;
And finally, the results of this study may not actually carry over to humans.
The bottom line is that it is far too soon to tell whether or not H pylori contributes to Parkinson’s, and we will not know until more research has been performed.
If you are still concerned about the possible links, be sure to discuss this with your doctor. Perhaps there may be some merit to testing for H pylori in the absence of symptoms if you are an otherwise healthy adult with a family history of Parkinson’s Disease. However, that should be a discussion between you and your doctor.
References
1. M.F. Salvatore, S.L. Spann, D.J. Mcgee, O.A. Senkovich, & T.L. Testerman. Helicobacter pylori infection induces Parkinson’s Disease symptoms in aged mice. Presentation at the 111th General Meeting for the American Society for Microbiology. 2011 May 22. New Orleans, LA.
Hi Krugen68
Very interesting indeed! I had seen a reference to the Helicobacter P. study but your text below is a lot more clear an instructive than what I saw - thanks.
In terms of relationship between gastro and Parkinson, I also found a very interesting french study from 2010. In essence they were able to diagnose PD (and to some extent the level of advance of the PD symptoms) just by looking at someone's intestines (doing a colon biopsy). The title of the paper is "Colonic Biopsies to Assess the Neuropathology of Parkinson’s Disease and Its Relationship with Symptoms" http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0012728 This paper does not make any statements regarding which side causes the other but it does establish a pretty convincing link between PD and the gastro system (and in particular the intestines).
I'm not sure yet what to make of this idea that Helicobacter P. may produces a neurotoxic compound that might kill off nerve cells... but am clearly interested in it (if anyone has more info on this I would appreciate). In the meantime I'm not yet discarding the other possible explanation that high or low gastric acidity levels (and it seems to be established that Helicobacter P. causes low gastric acid... though I guess the cause could possibly be something else too like ulcers, etc) may create absorption problems leading to deficiences in the key ingredients one needs as per my original post above. I should get my test results for the different Vit B levels in the next few days. If they don't come normal I'm going to ask my gastro-entorolgist to test stomach acidity levels to see if there's something in there. If there's nothing, at least that's one hypothesis I can close down and focus on the others.
Cheers,
lfs
Very interesting indeed! I had seen a reference to the Helicobacter P. study but your text below is a lot more clear an instructive than what I saw - thanks.
In terms of relationship between gastro and Parkinson, I also found a very interesting french study from 2010. In essence they were able to diagnose PD (and to some extent the level of advance of the PD symptoms) just by looking at someone's intestines (doing a colon biopsy). The title of the paper is "Colonic Biopsies to Assess the Neuropathology of Parkinson’s Disease and Its Relationship with Symptoms" http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0012728 This paper does not make any statements regarding which side causes the other but it does establish a pretty convincing link between PD and the gastro system (and in particular the intestines).
I'm not sure yet what to make of this idea that Helicobacter P. may produces a neurotoxic compound that might kill off nerve cells... but am clearly interested in it (if anyone has more info on this I would appreciate). In the meantime I'm not yet discarding the other possible explanation that high or low gastric acidity levels (and it seems to be established that Helicobacter P. causes low gastric acid... though I guess the cause could possibly be something else too like ulcers, etc) may create absorption problems leading to deficiences in the key ingredients one needs as per my original post above. I should get my test results for the different Vit B levels in the next few days. If they don't come normal I'm going to ask my gastro-entorolgist to test stomach acidity levels to see if there's something in there. If there's nothing, at least that's one hypothesis I can close down and focus on the others.
Cheers,
lfs
Sorry, just realized my link for the French study doesn't seem to work. If you're interested just google the title and you'll find it easily.
Hi
I may be wrong but I believe that no-one who has had an autopsy and been diagnosed as having parkinsons did not have damage to those specific neurons?
i believe that dopamine is produced this way:
soy, chicken, fish, peanuts etc include tyrosine amino acid (it can also be made from phenyalanine)
domapinergic cells convert tyrosine to levadopa by the enzyme TH (which can be increased by smoking)
levadopa is converted to dopamine by dopa decarboxlase (ddc) aka AAAD.
dopamine is later turned into norephinehrine and epinephrine
PDP (vit B6) is a coenzyme in the ldopa to dopamine step but is also involvded in many oher processes.
regulating systems keep all these chemicals in balance,i doubt it possible to change the balance by eating basic chemicals
that are likely to be used or eliminated before they get to the brain.
food => tyrosine => levadopa => dopamine
if i understand it right the only ingredient is the amino acid tyrosine.
the other enyzmes, co-enzymes etc are used in other processes so if they were defficient other neuro transmitters would be affected to.
toxicity from heliobacter is a different issue altogether and one i have experimented with myself.
the above may well all be misinterpreted by me.
one thing i dont get at all is if the missing cells convert ldopa to dopamine how does it work providing more ldopa? that would seem to imply a problem earlier in the process???
I may be wrong but I believe that no-one who has had an autopsy and been diagnosed as having parkinsons did not have damage to those specific neurons?
i believe that dopamine is produced this way:
soy, chicken, fish, peanuts etc include tyrosine amino acid (it can also be made from phenyalanine)
domapinergic cells convert tyrosine to levadopa by the enzyme TH (which can be increased by smoking)
levadopa is converted to dopamine by dopa decarboxlase (ddc) aka AAAD.
dopamine is later turned into norephinehrine and epinephrine
PDP (vit B6) is a coenzyme in the ldopa to dopamine step but is also involvded in many oher processes.
regulating systems keep all these chemicals in balance,i doubt it possible to change the balance by eating basic chemicals
that are likely to be used or eliminated before they get to the brain.
food => tyrosine => levadopa => dopamine
if i understand it right the only ingredient is the amino acid tyrosine.
the other enyzmes, co-enzymes etc are used in other processes so if they were defficient other neuro transmitters would be affected to.
toxicity from heliobacter is a different issue altogether and one i have experimented with myself.
the above may well all be misinterpreted by me.
one thing i dont get at all is if the missing cells convert ldopa to dopamine how does it work providing more ldopa? that would seem to imply a problem earlier in the process???
Hi Ifs,
I've fixed your link above and it should work fine now. Thanks for sharing this information.
Ezinda
I've fixed your link above and it should work fine now. Thanks for sharing this information.
Ezinda
Thanks Ezinda!
Hi Turnip,
Your point that autopsies have apparently demonstrated neuron damage in folks with PD seems to be correct (at least I have seen it mentioned elsewhere). The other "facts" that seems to be proven is that (a) DaTscans show lower level of dopamine transport activity and that (b) this level seems be around 25% of the normal level at the time folks get diagnosed with PD.
Now, I confess I don't know very well what this means exactly... but frankly I'm not going to jump to the easy (but not so re-assuring) conclusion that 75% of my dopaminic neurons are already dead and there's no way back. Before I accept that conclusion, I'd need to understand at least the following points(and would obviously welcome any insights anyone may have on any of them):
Point 1. As far as I can tell there seem to be 2 factors at play in the dopaminic neurons: (a) the creation and stockage of dopamine, and (b) the transmission of dopamine. But is this really correct?
Point 2. What exactly do the autopsies show? That the neurons that create and stock dopamine are dead? that they are unable to transport dopamine? or both?
Point 3. Do we know that dead neurons (or dead transport mechanisms, if that's what's at stake) are lost forever?
Your question at the end of your post a crucial one, I believe. My take is it is as follows:
A. Getting l-dopa supplements will help if one has a deficiency in creating l-dopa. This is why I'm trying to check my levels of every possible "ingredient" in the "formula" the brain uses to create l-dopa. My understanding is that these "ingredients" include: (a) l-tyrosine (the main one, as you indicated, and which apprently can be tested through a blood test), (b) THFA ("Tetrahydrofolic acid", which our body mainly creates from vit B9 though the "creation" process involves other aspects too); (c) Oxygen (which I personaly find a likely important one as PD has often been co-related with anemia and anemia = low oxygen in the blood); (d) ferrous iron; (e) something called Tyrosine hydroxylase, which apparently can go wrong due at least because of genetic deficiencies; and (f) something else called "Tetrahydro-biopterin" which I don't understand very well.
B. Getting l-dopa supplements may perhaps also boost the dopamine production rate of those remaining neurons that are still capable of producing it (sort of get's them to work at double speed as l-dopa is the main ingredient anyway). I have no clue if this is really true, but it seems a reasonable to me that it may be the case. This "boosting" logic may also apply if one has a problem with transforming L-dopa into dopamine (i.e., deficiency in PDP/vit B6 or problems with something called "Aromatic L-amino acid decarboxylase", which apparently can happen due to one's genetic make-up).
One last point, as you mention smoking. I don't smoke myself, but recall reading somewhere that the impact of smoking on dopamine is very short-lived (seconds? minutes?). So if anyone out there is thinking of increasing smoking to help boost dopamine, pls research that properly and consider the obvious drawbacks too. My grand father was a smoker and I watched him die when one day a blood clot got stuck somewhere in his brain. Not something I'd wish to anyone. I also presume that (emboly situations aside) smoking will generally reduce overal oxygenation levels (meaning it will reduce long-term L-dopa creation).
Good luck to all,
lfs
Hi Turnip,
Your point that autopsies have apparently demonstrated neuron damage in folks with PD seems to be correct (at least I have seen it mentioned elsewhere). The other "facts" that seems to be proven is that (a) DaTscans show lower level of dopamine transport activity and that (b) this level seems be around 25% of the normal level at the time folks get diagnosed with PD.
Now, I confess I don't know very well what this means exactly... but frankly I'm not going to jump to the easy (but not so re-assuring) conclusion that 75% of my dopaminic neurons are already dead and there's no way back. Before I accept that conclusion, I'd need to understand at least the following points(and would obviously welcome any insights anyone may have on any of them):
Point 1. As far as I can tell there seem to be 2 factors at play in the dopaminic neurons: (a) the creation and stockage of dopamine, and (b) the transmission of dopamine. But is this really correct?
Point 2. What exactly do the autopsies show? That the neurons that create and stock dopamine are dead? that they are unable to transport dopamine? or both?
Point 3. Do we know that dead neurons (or dead transport mechanisms, if that's what's at stake) are lost forever?
Your question at the end of your post a crucial one, I believe. My take is it is as follows:
A. Getting l-dopa supplements will help if one has a deficiency in creating l-dopa. This is why I'm trying to check my levels of every possible "ingredient" in the "formula" the brain uses to create l-dopa. My understanding is that these "ingredients" include: (a) l-tyrosine (the main one, as you indicated, and which apprently can be tested through a blood test), (b) THFA ("Tetrahydrofolic acid", which our body mainly creates from vit B9 though the "creation" process involves other aspects too); (c) Oxygen (which I personaly find a likely important one as PD has often been co-related with anemia and anemia = low oxygen in the blood); (d) ferrous iron; (e) something called Tyrosine hydroxylase, which apparently can go wrong due at least because of genetic deficiencies; and (f) something else called "Tetrahydro-biopterin" which I don't understand very well.
B. Getting l-dopa supplements may perhaps also boost the dopamine production rate of those remaining neurons that are still capable of producing it (sort of get's them to work at double speed as l-dopa is the main ingredient anyway). I have no clue if this is really true, but it seems a reasonable to me that it may be the case. This "boosting" logic may also apply if one has a problem with transforming L-dopa into dopamine (i.e., deficiency in PDP/vit B6 or problems with something called "Aromatic L-amino acid decarboxylase", which apparently can happen due to one's genetic make-up).
One last point, as you mention smoking. I don't smoke myself, but recall reading somewhere that the impact of smoking on dopamine is very short-lived (seconds? minutes?). So if anyone out there is thinking of increasing smoking to help boost dopamine, pls research that properly and consider the obvious drawbacks too. My grand father was a smoker and I watched him die when one day a blood clot got stuck somewhere in his brain. Not something I'd wish to anyone. I also presume that (emboly situations aside) smoking will generally reduce overal oxygenation levels (meaning it will reduce long-term L-dopa creation).
Good luck to all,
lfs
Researchers reveal role of protein mutation in Parkinson's diseaseTuesday, February 21, 2012
This is Fred Regnier. Credit: Purdue News Service Purdue University researchers revealed how a mutation in a protein shuts down a protective function needed to prevent the death of neurons in Parkinson's disease, possibly opening the door to new drug strategies to treat the disorder.
Fred Regnier, the J.H. Law Distinguished Professor of Chemistry, and Jean-Christophe Rochet, an associate professor of medicinal chemistry and molecular pharmacology, led the team that discovered how the protein DJ-1, which plays a significant role in protecting neurons from damage, is shut down by a subtle mutation.
A substitution in one link of the chain of amino acids that makes up the protein renders it unable to be activated to protect neurons from the build up of protein "aggregates," or "clumps," that lead to cell death in those with Parkinson's disease.
"The saying that you are only as strong as your weakest link appears to hold true in the case of the chain of amino acids that make up a protein," Regnier said. "The magnitude of the effect of this subtle change is surprising. It can make the difference between having a disease and being healthy."
According to the Parkinson's Disease Foundation, an estimated 7 million to 10 million people worldwide are living with the disease, which is a neurodegenerative disorder that causes muscular rigidity, slowness of movement, poor balance and tremors. The death of neurons in a region of the brain called the substantia nigra cause the symptoms.
The findings of the Purdue-led study could potentially lead to new Parkinson's treatments, Rochet said.
"The current methods of treatment are to add back what the lost cells used to produce, similar to hormone replacement therapies," he said. "Understanding this error in a key protein could help researchers find a way to prevent cell death in the first place. Perhaps a compound could be found that could correct the problem and resurrect the protective function of the protein. Of course interventions would be needed in many places to treat the disease, but this could be one of several places to target for a potential treatment."
When functioning properly, DJ-1 appears to serve as a "chaperone" protein for the neural protein alpha-synuclein, escorting and protecting it as it performs its biological task. Without the help of DJ-1, alpha-synuclein can unfold and expose sticky surfaces that cause it to clump together with other proteins. These clumps are a component of the "Lewy bodies" and other protein deposits that build up in the neurons of Parkinson's disease patients and cause the cells to die, he said.
About 10 years ago it was discovered that people with familial, early-onset Parkinson's disease had a mutation in the gene that encodes DJ-1 that leads to a mutant form of the protein through a substitution in one of the protein's amino acids.
The Purdue-led team developed a new quantitative mass spectrometry approach to evaluate and compare the mutant and normal protein. They discovered that the substitution prevents DJ-1 from undergoing an important chemical reaction in which oxygen is added to a specific site on the protein. This addition of oxygen takes the protein into a two-oxygen form that facilitates its chaperone function.
It had been thought that the amino acid substitution led to an unfolding of the protein, but the team found that it instead slightly alters the structure of the active site pocket, preventing the addition of oxygen at that site.
In addition the team found that the attachment of too much oxygen or an oxygen atom linked at the wrong location also disabled the protein's protective abilities, Rochet said.
"The interaction of this protein with oxygen needs to be very precise," Rochet said. "We need just enough oxygen added at just the right site to activate the protective ability of the protein, but too much oxygen or oxygen added at the wrong location causes real problems."
Because the precise oxidation of the protein may play a significant role in preventing the development of Parkinson's disease, evaluation of the levels of oxidized DJ-1, non-oxidized DJ-1 and over-oxidized DJ-1 could be the starting point of a new diagnosis method, Regnier said.
"Mass spectrometers could be used to find specific forms of DJ-1 and changes in the levels of these different forms could lead to a diagnosis of the disease," he said. "If we could find that a certain form or ratio appears early in disease development, we might be able to catch it and treat it earlier."
The team's findings are detailed in a paper in the February issue of the journal Molecular and Cellular Proteomics. In addition to Regnier and Rochet, paper co-authors include postdoctoral research associate Ashraf G. Madian and graduate student Naomi Diaz-Maldonado of the Purdue Department of Chemistry; graduate students Jagadish Hindupur and Vartika R. Mishra and former graduate student John D. Hulleman of the Purdue Department of Medicinal Chemistry and Molecular Pharmacology; and Emmanuel Guigard and Cyril M. Kay from the Department of Biochemistry at the University of Alberta, Canada.
###
This is Fred Regnier. Credit: Purdue News Service Purdue University researchers revealed how a mutation in a protein shuts down a protective function needed to prevent the death of neurons in Parkinson's disease, possibly opening the door to new drug strategies to treat the disorder.
Fred Regnier, the J.H. Law Distinguished Professor of Chemistry, and Jean-Christophe Rochet, an associate professor of medicinal chemistry and molecular pharmacology, led the team that discovered how the protein DJ-1, which plays a significant role in protecting neurons from damage, is shut down by a subtle mutation.
A substitution in one link of the chain of amino acids that makes up the protein renders it unable to be activated to protect neurons from the build up of protein "aggregates," or "clumps," that lead to cell death in those with Parkinson's disease.
"The saying that you are only as strong as your weakest link appears to hold true in the case of the chain of amino acids that make up a protein," Regnier said. "The magnitude of the effect of this subtle change is surprising. It can make the difference between having a disease and being healthy."
According to the Parkinson's Disease Foundation, an estimated 7 million to 10 million people worldwide are living with the disease, which is a neurodegenerative disorder that causes muscular rigidity, slowness of movement, poor balance and tremors. The death of neurons in a region of the brain called the substantia nigra cause the symptoms.
The findings of the Purdue-led study could potentially lead to new Parkinson's treatments, Rochet said.
"The current methods of treatment are to add back what the lost cells used to produce, similar to hormone replacement therapies," he said. "Understanding this error in a key protein could help researchers find a way to prevent cell death in the first place. Perhaps a compound could be found that could correct the problem and resurrect the protective function of the protein. Of course interventions would be needed in many places to treat the disease, but this could be one of several places to target for a potential treatment."
When functioning properly, DJ-1 appears to serve as a "chaperone" protein for the neural protein alpha-synuclein, escorting and protecting it as it performs its biological task. Without the help of DJ-1, alpha-synuclein can unfold and expose sticky surfaces that cause it to clump together with other proteins. These clumps are a component of the "Lewy bodies" and other protein deposits that build up in the neurons of Parkinson's disease patients and cause the cells to die, he said.
About 10 years ago it was discovered that people with familial, early-onset Parkinson's disease had a mutation in the gene that encodes DJ-1 that leads to a mutant form of the protein through a substitution in one of the protein's amino acids.
The Purdue-led team developed a new quantitative mass spectrometry approach to evaluate and compare the mutant and normal protein. They discovered that the substitution prevents DJ-1 from undergoing an important chemical reaction in which oxygen is added to a specific site on the protein. This addition of oxygen takes the protein into a two-oxygen form that facilitates its chaperone function.
It had been thought that the amino acid substitution led to an unfolding of the protein, but the team found that it instead slightly alters the structure of the active site pocket, preventing the addition of oxygen at that site.
In addition the team found that the attachment of too much oxygen or an oxygen atom linked at the wrong location also disabled the protein's protective abilities, Rochet said.
"The interaction of this protein with oxygen needs to be very precise," Rochet said. "We need just enough oxygen added at just the right site to activate the protective ability of the protein, but too much oxygen or oxygen added at the wrong location causes real problems."
Because the precise oxidation of the protein may play a significant role in preventing the development of Parkinson's disease, evaluation of the levels of oxidized DJ-1, non-oxidized DJ-1 and over-oxidized DJ-1 could be the starting point of a new diagnosis method, Regnier said.
"Mass spectrometers could be used to find specific forms of DJ-1 and changes in the levels of these different forms could lead to a diagnosis of the disease," he said. "If we could find that a certain form or ratio appears early in disease development, we might be able to catch it and treat it earlier."
The team's findings are detailed in a paper in the February issue of the journal Molecular and Cellular Proteomics. In addition to Regnier and Rochet, paper co-authors include postdoctoral research associate Ashraf G. Madian and graduate student Naomi Diaz-Maldonado of the Purdue Department of Chemistry; graduate students Jagadish Hindupur and Vartika R. Mishra and former graduate student John D. Hulleman of the Purdue Department of Medicinal Chemistry and Molecular Pharmacology; and Emmanuel Guigard and Cyril M. Kay from the Department of Biochemistry at the University of Alberta, Canada.
###
I am sure there is some neuro somewhere reading this and rolling around the floor, but what the hell!
Yep most of those neurons are gone but the body's ever so clever regulatory systems compensates for years by various means so its not so obvious.
One line of research is to replace those cells with new ones - a great idea but there are considerable difficulties.
I think (ie wikipedia) that it goes like this-
the SN cells manufacture dopamine,(The other main area that does that is the VTA)
the dopamine travels along dopaminergic pathways (there are 4) from the SN or VTA to the areas that use it. I believe the dopamine cells have long axions which reach to their destination areas. I think the transportation neuron is the same as the manufacturing. i am not sure whether the dopamine is added to the receiving cell through the cell wall but i suspect it is.
I am definitely not saying take up smoking!
good luck with your investigations!
K68 thanks for that, it really looks like the researchers are targetting in on the details. hopefully with treatments following.
Yep most of those neurons are gone but the body's ever so clever regulatory systems compensates for years by various means so its not so obvious.
One line of research is to replace those cells with new ones - a great idea but there are considerable difficulties.
I think (ie wikipedia) that it goes like this-
the SN cells manufacture dopamine,(The other main area that does that is the VTA)
the dopamine travels along dopaminergic pathways (there are 4) from the SN or VTA to the areas that use it. I believe the dopamine cells have long axions which reach to their destination areas. I think the transportation neuron is the same as the manufacturing. i am not sure whether the dopamine is added to the receiving cell through the cell wall but i suspect it is.
I am definitely not saying take up smoking!
good luck with your investigations!
K68 thanks for that, it really looks like the researchers are targetting in on the details. hopefully with treatments following.
A response to my posting on DJ-1 in the US, anyone here tried the supplement ?
The cheapest I can buy it is in the States
http://neurotalk.psychcentral.com/thread165444.html
PQQ protects against the self-oxidation of the DJ-1 gene. Pyrroloquinoline quinone (PQQ) is available as a supplement
The cheapest I can buy it is in the States
http://neurotalk.psychcentral.com/thread165444.html
PQQ protects against the self-oxidation of the DJ-1 gene. Pyrroloquinoline quinone (PQQ) is available as a supplement
Hi Turnip and Krugen68,
Thanks for the good info from both. Lots of food for thought there !
The idea of PQQ supplements seems an interesting one (will surely look more into that one). Any info on what are the potencies/quantities that make sense?
In terms of US suppliers (cf. your other post), while I don't have experience with PQQ supplements, I can say that I've been buying my CoQ10 and Vit E supplements from VitaCost (US) and am happy with them: a) they seem to be pretty cheap (compared with other US suppliers I looked); (b) they sell the pills with the exact potencies I was looking for (e.g., 400 mg for CoQ10, which isn't that widely available); and (c) the pills seem to be doing their job (i.e., my blood levels of CoQ10 and Vit 10 are now pretty high). I've just looked and they seem to sell bottles of 30 PQQ pills of 10 mg each for $18.00... but again, I have no idea what potencies/quantites we should be interested in and don't know much about other US suppliers.
regards,
lfs
Thanks for the good info from both. Lots of food for thought there !
The idea of PQQ supplements seems an interesting one (will surely look more into that one). Any info on what are the potencies/quantities that make sense?
In terms of US suppliers (cf. your other post), while I don't have experience with PQQ supplements, I can say that I've been buying my CoQ10 and Vit E supplements from VitaCost (US) and am happy with them: a) they seem to be pretty cheap (compared with other US suppliers I looked); (b) they sell the pills with the exact potencies I was looking for (e.g., 400 mg for CoQ10, which isn't that widely available); and (c) the pills seem to be doing their job (i.e., my blood levels of CoQ10 and Vit 10 are now pretty high). I've just looked and they seem to sell bottles of 30 PQQ pills of 10 mg each for $18.00... but again, I have no idea what potencies/quantites we should be interested in and don't know much about other US suppliers.
regards,
lfs
.....they appear to recommend 10mg to 20mg per day, some interesting feedback on non-pd sites about pqq(bodybuilders try anything 
)
How do you get your COQ10 and vitamin levels measured ? ( I was taking 1200mg of COQ10 per day )
)How do you get your COQ10 and vitamin levels measured ? ( I was taking 1200mg of COQ10 per day )
PQQ
Just bought 3 bottles pqq x 30 10mg capsules (total 90 capsules) for £36.88 (free post) on amazon uk
Just bought 3 bottles pqq x 30 10mg capsules (total 90 capsules) for £36.88 (free post) on amazon uk
Wow - so much for the myth that everything is cheaper in the US :-)
Here's how I go about measuring these things (note that I live in Belgium - so not sure if all applies the same for the UK):
1. Google + "deficiency diagnosis" (and/or "overload diagnosis") to see what tests exist. So far, I found that the following can be done through blood/urine testing: vit B3, vit B6, folic acid (vit B9), Vit B12, Vit E, Vit D, CoQ10, Manganese, Iron, Zinc, Lead, L-Dopa, L-tyrosine, L-phenylalanine and Phenylalanine Hydroxylase. However, note that these obviously only measure the level of the stuff in the blood/urine which is not always what are looking for (but I'm hoping a good enough proxy). Also note that some are tricky : I was told this morning that measuring Acid folic is not a good proxy for THFA (not sure I understand the logic of what I was told just yet). So far I've done vit B6, folic acid (vit B9), Vit B12, Vit E, Vit D, CoQ10, Manganese, Iron, and Zinc. So I'm sure these are possible.
2. Find a lab that does it (and do this before step 3 whenever you can). I just scan their internet sites and/or called them and ask... Also be carefull because I got a few times cases where the person that answers the phone says "yes, no problem" and when I got the results back it was written on the page "sorry, we don't do this test". So double/triple check if you can otherwise it's just a huge waist of time & money.
3. Get a prescription. This is the most difficult and time consuming part. In my case: (a) My neurologist doesn't care about this type of things - other than for Vit D(which she knows for sure PD patients are often deficient in); (b) my 2nd move was to call a GP (just picked up one from the yellow pages), scheduled an appointment and explain that I had PD and was taking very large doses of supplements (CoQ10 and Vit E) and asked her help to monitor levels so I wouldn't go overboard with it. I presume any GPs should always be symphatetic with this line of argument ... and she did. Only problem is that she had never heard of COQ10 nor obviously knew where to do the test (which is why step 2 before makes sense). Also think of bringing a copy of the study that showed that CoQ10 had good results with PD to re-assure her/him you're not just crazy. In my case, she gave me the prescription for CoQ10 and Vit E without problems. This approach will probably work for most vitamins and CoQ10 but won't likely work for the stuff more directly linked with PD; (c) For that more sophisticated stuff (L-dopa, L-tyrosine, L-phenylalanine and Phenylalanine Hydroxylase) it's more difficult as GPs will probably be reluctant to get involved. I haven't been able to test them yet but trying two things: I'm getting an appointment with a neurologist from a reasearch university (but long wait list - so not yet done), and I ask in the lab where they do the tests for a name of a doctor that does them often. They gave me the name of a nutricionist which I saw today and who seems happy to go down that path with me (although he didn't just prescribe the list of stuff I asked him... but that's obviously normal).
4. Also, when I get a prescription I insist that the doctor writes in there "give a copy of the results to the patient" as here if you don't have that the lab will refuse to show you the results ... and you loose more time.
Hope this helps,
lfs
Here's how I go about measuring these things (note that I live in Belgium - so not sure if all applies the same for the UK):
1. Google
2. Find a lab that does it (and do this before step 3 whenever you can). I just scan their internet sites and/or called them and ask... Also be carefull because I got a few times cases where the person that answers the phone says "yes, no problem" and when I got the results back it was written on the page "sorry, we don't do this test". So double/triple check if you can otherwise it's just a huge waist of time & money.
3. Get a prescription. This is the most difficult and time consuming part. In my case: (a) My neurologist doesn't care about this type of things - other than for Vit D(which she knows for sure PD patients are often deficient in); (b) my 2nd move was to call a GP (just picked up one from the yellow pages), scheduled an appointment and explain that I had PD and was taking very large doses of supplements (CoQ10 and Vit E) and asked her help to monitor levels so I wouldn't go overboard with it. I presume any GPs should always be symphatetic with this line of argument ... and she did. Only problem is that she had never heard of COQ10 nor obviously knew where to do the test (which is why step 2 before makes sense). Also think of bringing a copy of the study that showed that CoQ10 had good results with PD to re-assure her/him you're not just crazy. In my case, she gave me the prescription for CoQ10 and Vit E without problems. This approach will probably work for most vitamins and CoQ10 but won't likely work for the stuff more directly linked with PD; (c) For that more sophisticated stuff (L-dopa, L-tyrosine, L-phenylalanine and Phenylalanine Hydroxylase) it's more difficult as GPs will probably be reluctant to get involved. I haven't been able to test them yet but trying two things: I'm getting an appointment with a neurologist from a reasearch university (but long wait list - so not yet done), and I ask in the lab where they do the tests for a name of a doctor that does them often. They gave me the name of a nutricionist which I saw today and who seems happy to go down that path with me (although he didn't just prescribe the list of stuff I asked him... but that's obviously normal).
4. Also, when I get a prescription I insist that the doctor writes in there "give a copy of the results to the patient" as here if you don't have that the lab will refuse to show you the results ... and you loose more time.
Hope this helps,
lfs
hi ifs
i think you have a problem measuring l-dopa in the urine as dopamine is made and used in the kidneys (which are rather closer to urine production) so you would almost certainly not get an accurate picture of the levels in the brain. As always I might be totally wrong.
have you found any interesting results from your tests so far?
i think you have a problem measuring l-dopa in the urine as dopamine is made and used in the kidneys (which are rather closer to urine production) so you would almost certainly not get an accurate picture of the levels in the brain. As always I might be totally wrong.
have you found any interesting results from your tests so far?
Hi turnip
You may be right about measuring l-dopa in the urine not being useful. At least the doctor I saw yesterday seemed to think the same thing. I confess I don't fully understand why yet (I was hoping that if the test results would be ok it would at least tell me that my body was capable of getting all the ingredients to make it and there was nothing wrong with my genetic makeup that is involved in the process).
In what concerns my own situation, my findings so far are that:
1. I'm low on vit D (but I don't see any relevance in this so far).
2. I'm high on CoQ10 and Vit E but that's normal given I'm taking supplements
3. I seem to be a bit high on vit B1 and acid folic (vit B9) which is
surprising to me and I don't know what it means yet (I was expecting to be
low on folic acid).
3. I seem to be low on iron (though not fully clear). I tested iron twice so
far. In the first test it was low. In the second was normal but the iron-to-
transferin ratio was low (I believe this measures the level of iron
transported in the blood - thus what is effectivelly delivered to cells).
And the relative measure of % of transferrin saturation (iron / TIBC) was
also low.
4. I'm high on ferritine (which seems to measure acumulated iron). My
explanation for this is that I have an infection somewhere (which
apparently makes ferritine levels raise)
5. My hemoglobine level is on the low end of normal (but technically not in the
anemia range)
6. My MCV (red blood cell size) and MCH (hemoglobine per cell) are low.
According to our good friend google this could be explained by: iron
deficiency, lead poisoning, anemia (plus a few other things I find
unlikely). The lead poisoning part could be important to me as I have a
small lead bullet in my arm (from playing with an air pressure gun when a
child). I always thought this was not a big deal... but not so sure anymore
when I realized it may be showing in my blood. I'm definitelly going to
check this one further.
6. I'm high on cholesterol
7. I have had some occasional cardiac arrhythmias in the past and my blood
pressure is generally on the low side.
8. I tested positive for H. Pylori 12 years ago (but negative recently).
So, my top hypotheses so far are that my PD may somewhat be linked to (perhaps a combination of):
A. Low iron (which itself may be due low gastric acid or absorption problems).
B. Infection (not sure where - maybe the lead bullet; maybe something gastric)
C. Lead exposure
D. H. Pylori
E. Oxygen problems (I'm less convinced about this one, but maybe the arrhythmias
combined with low blood pressure, cholesterol, and relative low hemoglobine
do have an impact in the oxygen that makes it to the brain).
BTW, one thing that I found helpful was putting the results of all the blood & urine tests I have done in the past 20 years on an excell spreasheet (in my case I have a dozen from regular check-ups I did once in a while) and just highlight (bold/color/etc) the results that were out of norm. My low MCV and MCH for example got highlighted in all tests except one (and no medical doctor that saw them ever thought they could be any problem).
Cheers,
lfs
You may be right about measuring l-dopa in the urine not being useful. At least the doctor I saw yesterday seemed to think the same thing. I confess I don't fully understand why yet (I was hoping that if the test results would be ok it would at least tell me that my body was capable of getting all the ingredients to make it and there was nothing wrong with my genetic makeup that is involved in the process).
In what concerns my own situation, my findings so far are that:
1. I'm low on vit D (but I don't see any relevance in this so far).
2. I'm high on CoQ10 and Vit E but that's normal given I'm taking supplements
3. I seem to be a bit high on vit B1 and acid folic (vit B9) which is
surprising to me and I don't know what it means yet (I was expecting to be
low on folic acid).
3. I seem to be low on iron (though not fully clear). I tested iron twice so
far. In the first test it was low. In the second was normal but the iron-to-
transferin ratio was low (I believe this measures the level of iron
transported in the blood - thus what is effectivelly delivered to cells).
And the relative measure of % of transferrin saturation (iron / TIBC) was
also low.
4. I'm high on ferritine (which seems to measure acumulated iron). My
explanation for this is that I have an infection somewhere (which
apparently makes ferritine levels raise)
5. My hemoglobine level is on the low end of normal (but technically not in the
anemia range)
6. My MCV (red blood cell size) and MCH (hemoglobine per cell) are low.
According to our good friend google this could be explained by: iron
deficiency, lead poisoning, anemia (plus a few other things I find
unlikely). The lead poisoning part could be important to me as I have a
small lead bullet in my arm (from playing with an air pressure gun when a
child). I always thought this was not a big deal... but not so sure anymore
when I realized it may be showing in my blood. I'm definitelly going to
check this one further.
6. I'm high on cholesterol
7. I have had some occasional cardiac arrhythmias in the past and my blood
pressure is generally on the low side.
8. I tested positive for H. Pylori 12 years ago (but negative recently).
So, my top hypotheses so far are that my PD may somewhat be linked to (perhaps a combination of):
A. Low iron (which itself may be due low gastric acid or absorption problems).
B. Infection (not sure where - maybe the lead bullet; maybe something gastric)
C. Lead exposure
D. H. Pylori
E. Oxygen problems (I'm less convinced about this one, but maybe the arrhythmias
combined with low blood pressure, cholesterol, and relative low hemoglobine
do have an impact in the oxygen that makes it to the brain).
BTW, one thing that I found helpful was putting the results of all the blood & urine tests I have done in the past 20 years on an excell spreasheet (in my case I have a dozen from regular check-ups I did once in a while) and just highlight (bold/color/etc) the results that were out of norm. My low MCV and MCH for example got highlighted in all tests except one (and no medical doctor that saw them ever thought they could be any problem).
Cheers,
lfs