Hello,

It’s been a few weeks since I posted something on my first post with the same title http://bit.ly/HbRYNk , so thought I might give a quick update to those of you that may be interested - and ask for any further suggestions or ideas any of you may have.

Since my previous post I’ve essentially got a new set of lab analyses results and had a few discussions with various medical doctors. Here’s a quick update from the things I learned:

1. Mercury poisoning. Like some of you I was concerned that the mercury in my teeth fillings might be a possible cause of my PD. Well, my blood and urine tests show that my mercury levels in my blood and urine are pretty normal. So, if there’s any mercury poisoning going on, it’s not significant enough to show there. I’m thus putting this hypothesis on “low probability”.

2. Iron deficiency. I’m increasingly doubting that this one is a concern as well. As I mentioned before, one of my blood tests showed a low level of iron, but the two subsequent ones showed an ok level. Also, in some of these my ferritin levels were a bit above norm and ferritin seem to be a more accurate measure of iron (measures the iron that is accumulated in the cells). Even if we take into account that high ferritin can also be explained by infection (which I do suspect), the doctors I have discussed this with say that they really see no evidence elsewhere of iron deficiency. So, I’m moving this one to the “med/low probability” category.

3. Oxygen deficiency. As I mentioned in my earlier posts, I suspected this one too, but my neurologist thinks it is unlikely. She argues that if neurons in the PD-relevant areas are dying because of lack of oxygen then one would see it in the IRM (and my IRMs don’t show it). Even though IRMs don’t apparently catch everything, she does have a point. I’m downgrading this one too to the “med/low probability” category too.

4. Infection/inflammation. I continue to keep this one as a “high probability”. My ferritin levels being higher than my iron levels is one reason. I also have a few other lab results that are consistent with it. Still I have made no great progress on finding where the infection/inflammation comes from, but my recent results raised one interesting possibility that I hadn’t thought of before – that I may be low on two things that apparently have anti-inflammatory properties: unbound cortisol and on Gamma-Linolenic Acid (GLA). I’m not too sure yet on what’s the best thing to do about these (and there might be more in that than meets the eye - see below), so any insights would be welcomed.

5. THFA deficiency (Tetrahydrofolic acid). If you can remember these wonderful medical names, you may remember that this thing is rather important for PD (is necessary for the brain to make dopamine on its own, and when we lack it our brains end up creating something else that destroys the neurons instead – thus very consistent with PD). THFA is mainly made up of folic acid (vit B9) and my folic acid levels seemed to be ok, so I thought I was good on THFA. Interestingly, THFA deficiency seems to be one of the possible causes of why someone can be low on unbound cortisol and on gamma linolenic acid (the two things I mention above I’m low on). I’m thus putting THFA deficiency back on my "high probability" category and am trying to find a way to confirm if yes or no I have some THFA problems (despite having an ok level of folic acid). So far, I haven’t manage to understand how one can really test this THFA thing, so would also welcome any insight that any of you might have on this too.

Warm regards to all and please do let me know if you have any thoughts or suggestions on any of the above,

lfs

i posted this is the middle of another thread. i hope no-one minds a repition. personaslly i think its very illuminating but thats probably because it agrees with my own bias.
http://www.hindawi.com/journals/pd/2011/713517/

"The present paper will focus upon the evidence linking microglia and their inflammatory processes to the death of DA neurons following toxin exposure. Particular attention will be devoted to the possibility that environmental toxins can activate microglia, resulting in these cells adopting a “sensitized” state that favors the production of proinflammatory cytokines and damaging oxidative radicals."

in other words there is an initial cause eg poison exposure, which then sets up the 'dustbin-men' cells (microglia) to misbehave much later when a trigger occurs, such as an infection or stress. instead of just tidying up they cause more damage (cytokines, oxidative radicals) which causes more tidying-up - a vicious circle. so the original cause may have been unnoticed and have completely gone leaving a potential mess behind. the question is then how to get the dustbin-men back on track.

then again its just an article amongst hundreds.

ps that fits in with option 4

Noted above, I noticed when working that ladies with PD type illness had really fine white skin, like myself, and I thought at that time I would be likely to get PD. Turnip mentioned skin and immune system. Also I always have had a very soft voice so I think the PD factor was there from birth. Possibly chemical exposure came later.

i know there are several of us who think we can trace back symptoms 30 years or more, but its impossible to prove. i went to a physio when i was 25 and was told i had 'the tightest calve muscles' he had ever come across. they are still my main problem and now definitely pd.

Hi Turnip

I was away for several days with no internet access but just wanted to say "thanks" for your article above. I'm not sure I understand the full thing yet (getting lost in the huge number of obscure medical acronyms) but clearly there's something in there - I'll need to spend more time "decyphering it".

Also, just in case you haven't seen it yet, I happened to browse through one of the articules referred to by your article and thought it was quite enlightening as well, as presents things in closer to plain english and has a section discussing possible treatments for inflammation (something that I'm getting more and more interested in as you can see below ) - you can find it here: http://masterneuro.univ-mrs.fr/IMG/pdf/LancetNeurol-09-8-382.pdf

... and if the link doesn't work, just google the title "Neuroinflammation in Parkinson’s disease: a target for neuroprotection? masterneuro". Note that the last word is the name of the website where you can find it for free.

Also, in the meantime, I received the results from my genetic testing (from www.23andMe.com). Not sure I understand it well yet, but my reading so far is that:

a. They didn't detect any genetic factor that they normally associate with a higher likelihood of PD (so they seem me as an average likelihood of getting PD).

b. They did list a number of conditions that my genetic make-up makes me more likely to get (at least based on correlation studies they did). The one they list with the highest probability is "type 2 diabetes", but I'm not sure this one is the most interesting one as they also say it's very likely for everybody - my genetic makeup apparently just makes it slightly higher probability than average. Perhaphs more interestingly is that most of the other conditions they list me as having a higher-than-average probability of getting are about inflammations/infections in the gastro-intestinal system (crown disease, stomach cancer, ulcerative colitis, and esophageal cancer). I just went through a rather exhaustive gastro-intestinal system check-up in the past few months and nothing abnormal was unconvered, but the fact that I seem to be more inflammation-prone from a genetic perspective lends credibility that chronic inflammation may be behind my PD.

I'm thus moving my hypothesis #4 above to a high probability... and think I'll start investigating anti-inflammatory options.

Best regards to all,

lfs

As a now retired academic, teaching chemistry and Forensics.
I am convinced that my working lab. environment initiated my Parkinsons (dx Aug 2009)

Mainly the solvents carbon disulphide, Carbon tetrachloride and trichlorethylene.

Independant research has linked this group as possible causal effects triggering P.

Hi Frosty
Its good to have person with a scientific background participating (unlike myself). As I presume you are no longer in contact with those chemicals, do you have a view as to how the process continues - are they toxins still in your system, have they set of an immune response etc?
From my own point of view, if I say anything daft, corrections are most welcome (other than spelling).
cheers

Hi Frosty,

Thanks for sharing. I too have no medical/chemical background and thus no clue on how these solvents might work for PD. Is there something that you think can be done in these cases to attenuate or seek to reverse the impact? Also, have you been able to find any way to sort of "validate/confirm" that causuality?

Warm regards,

lfs

Turnip & Ifs.


As said, I have used extensively solvents such as carbon disulphide etc..``
Quite a few scientific papers have been published, indicating that such solvents, pesticides,herbicides could be a causal factor in triggering the demise of dopamine producing neurons..

A good web site, which lists the various potential neurological toxins can be found here...........
http://viartis.net/parkinsons.disease/toxic.causes.htm