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.

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

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

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

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.

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

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???

Hi Ifs,
I've fixed your link above and it should work fine now. Thanks for sharing this information.

Ezinda