Parkinson's Disease Tulip


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Old 06-02-2012, 11:24 AM #1
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Default Can we slow PD progression rates by moving house?

I ask the question: Is it possible to slow the rate of progression of PD by moving house?

To set the scene for what follows, let me say that I think that there are many types of PD, with each modulated by genetics unique to the individual. So what follows will not apply to everyone.

Suppose that there is a subgroup of PwP whose PD is made to progress by environmental toxins, either man-made or natural.

Suppose, also, that the toxin load varies from place to place: house to house, neighbourhood to neighbourhood, county to county etc..

If these two conditions apply, we can affect the rate of progression by moving house. In particular, we could slow the rate of progression by moving to PD friendly houses or areas.

How would we recognise such places?

Ideally we would have assessments specific to each house. For instance, they could include a chemical analysis of the water supply. Unfortunately, not only would this be expensive but, except for some gross features, we don't know what we are looking for - after all the aetiology of PD is unknown.

Second best would be geographically based measures of disease progression rates. I've not been able to find such statistics. Hopefully, initiatives such as PPMI, will yield such data in the future. But, until then, how can we estimate progression rates with the available data?

I think most people would agree that PD usually has a pre-symptomatic phase lasting several years, where damage is being done to the brain, but without visible effect. And following this there is often a period of several more years of minor symptoms before the PwP presents him/herself to a doctor. This is often followed by another delay before a diagnosis of PD is made. Let's call these times taken together the prediagnosis period.

The prediagnosis period will be longer in areas of slow progression than in areas of fast progression. So, we would expect the average age of diagnosis to be lower in areas of fast progression.

The next approach that comes to mind is that places with slow progression should have a low disease incidence. But, since we are only slowing the progression, not stopping it, and assuming we are in steady state, the difference in incidence rates is limited to the difference in the number of people who died following an early PD diagnosis, rather than following a late PD diagnosis.

Has anyone experienced a changed rate of progression after moving to a different house or area?

John
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Born 1955. Diagnosed PD 2005.
Meds 2010-Nov 2016: Stalevo(75 mg) x 4, ropinirole xl 16 mg, rasagiline 1 mg
Current meds: Stalevo(75 mg) x 5, ropinirole xl 8 mg, rasagiline 1 mg
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Old 06-02-2012, 05:06 PM #2
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JohnT-
Some environmental factors to work in neuroinflammation as a common feature-
1) Nanoparticles from diesel exhaust seems to have made areas of Mexico City a place of keen interest for PD research. See
Air pollution & the brain: Subchronic diesel exhaust exposure causes neuroinflammation and elevates early markers of neurodegenerative disease.

Levesque S, Surace MJ, McDonald J, Block ML.
J Neuroinflammation. 2011 Aug 24;8:105.
PMID:
21864400
[PubMed - indexed for MEDLINE]
Free PMC Article
Related citations
2.
Effect of prolonged exposure to diesel engine exhaust on proinflammatory markers in different regions of the rat brain.

Gerlofs-Nijland ME, van Berlo D, Cassee FR, Schins RP, Wang K, Campbell A.
Part Fibre Toxicol. 2010 May 17;7:12.
PMID:
20478040
[PubMed - indexed for MEDLINE]
Free PMC Article
Related citations
3.
Nanometer size diesel exhaust particles are selectively toxic to dopaminergic neurons: the role of microglia, phagocytosis, and NADPH oxidase.

Block ML, Wu X, Pei Z, Li G, Wang T, Qin L, Wilson B, Yang J, Hong JS, Veronesi B.
FASEB J. 2004 Oct;18(13):1618-20. Epub 2004 Aug 19.
PMID:
15319363
[PubMed - indexed for MEDLINE]
Free Article
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Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 06-02-2012, 06:50 PM #3
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You could do some searching and see if there are any state or gov maps on various possible toxins or pollutants in your loaction. Then you would have a better idea as to what might be in your area and worth testing for.


Here is one for Radon- some larger cities might have a more detailed map for it.
Red is highest amounts
Orange is moderate
Yellow is low
http://www.epa.gov/radon/pdfs/zonemapcolor.pdf

I'm sure other countries have something similar listed under the governmental environment section.
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Old 06-04-2012, 04:36 AM #4
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My thanks to Rick and Jo*mar for for their postings on the effect of diesel exhaust and radon, respectively.

The paper by Willis et al. [1] shows geographical differences in prevalence and incidence rates for PD. And I've posted that these correlate with the geographical distribution of toxins such as nitric oxide, surface ozone and histoplasma.

I think that most people would accept that environmental toxins play a role in the aetiology of PD.

It is the next step that interests me here: can a PwP make use of this information?

It comes down to your view of the aetiology of your version of PD.

I take it for granted that there is a genetic component to PD, but beyond that there are a number of ways the environment could affect the outcome.

A single toxin assault could kill off enough dopaminergic neurons to give PD symptoms. This could be immediate or gradual. Or the assaualt could trigger an immune response that leads inexorably to insufficient dopamine being produced. But, each way, if this were the case, by the time of PD diagnosis turning off the toxin assault by moving house, or other means, would make no difference to progression rates.

Alternatively, there may be a form of the disease where the damage is done at a rate linked to the size of the instantaneous toxin assault: when the toxin assault is strong, progression is fast; when the toxin assault is weak, progression is slow. In this case, reducing the toxin flow, would reduce the rate of progression. Ideally, we would like to reduce the toxin load directly, for instance by changing diet or filtering the air etc.. But, since we don't know what causes PD, we don't know what to change. However, the fact that we don't have this direct knowledge, doesn't mean that we can do nothing. We could move to those areas where the epidemiological evidence shows that progression rates are low.

I live about 2 miles east of a major motorway, M6. The section near Stafford is used by over 100,000 vehicles per day. The prevailing wind blows the diesel exhaust that Rick mentions towards me.

Do I move?

Would you move house if you thought the rate of progression would be reduced by 10%?

Would you move house if you thought the rate of progression would be halved?

Has anyone found that air filtering has made a diference?

[1] "Geographic and Ethnic Variation in Parkinson Disease: A Population-Based Study of US Medicare Beneficiaries"
Allison Wright Willis, Bradley A. Evanoff, Min Lian, Susan R. Criswell, and Brad A. Racette
Neuroepidemiology. 2010 April; 34(3); 143-151.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2865395/

John
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Meds 2010-Nov 2016: Stalevo(75 mg) x 4, ropinirole xl 16 mg, rasagiline 1 mg
Current meds: Stalevo(75 mg) x 5, ropinirole xl 8 mg, rasagiline 1 mg
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Old 06-04-2012, 09:14 AM #5
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[QUOTE=johnt;885405]friendly houses or areas.

How would we recognise such places?

Has anyone experienced a changed rate of progression after moving to a different house or area?

John[/QUOTE

Hi John,

I feel particularly drawn to this subject (Cancerian of course )- I have repetitive dreams about homes - generally these dreams present clutter, old furniture, loong dark hallways, many floors and dilapidated doors. Considering especially the quantum model of epigenetics (genes can be triggered off and on by feelings) my philosophy is to focus more on what makes me well rather than postulate how I got sick - so many elements coming together cyclically or at once its all dynamic and the forest fire even if started with a single match is already burned down.

I think you are so on target with the importance of good water!! I wonder if altitude might also be a factor. I moved near Glacier Park Montana for a year and did exceptionally well - better in many ways. I was surrounded by pristine and magnificent beauty-and pd sx lessened indeed.

GREAT THREAD!

all the best to you
md
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Last edited by moondaughter; 06-04-2012 at 10:43 AM.
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Old 06-09-2012, 09:11 PM #6
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Moondaughter, thanks for raising the issue of altitude. I'm looking into it.

My thanks go to GerryW for pointing out the paper by Qin et al. [1]. They write:

"LPS reduced the number of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra (SN) by 23% at 7-months post-treatment, which progressed to 47% at 10 months.Together, these data demonstrate that through TNFalpha, peripheral inflammation in adult animals can: (1) activate brain microglia to produce chronically elevated pro-inflammatory factors; (2) induce delayed and progressive loss of DA neurons in the SN. These findings provide valuable insight into the potential pathogenesis and self-propelling nature of Parkinson's disease."

The key word here is "self-propelling". I take this to mean that a single environmental hit can set off an immune system response that cannot be stopped purely by ensuring there are no more environmental hits. So, if this is true of your type of PD, moving - even to the perfect location - will not, in itself, stop progression.

But can moving slow progression?

This will depend on whether new toxins add to the rate at which damage is done. Does anyone have any information on this?

[1] "Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration."
Qin L, Wu X, Block ML, Liu Y, Breese GR, Hong JS, Knapp DJ, Crews FT
Glia. 2007 Apr;55(5):453-62.
http://www.ncbi.nlm.nih.gov/pubmed/17203472

John
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Meds 2010-Nov 2016: Stalevo(75 mg) x 4, ropinirole xl 16 mg, rasagiline 1 mg
Current meds: Stalevo(75 mg) x 5, ropinirole xl 8 mg, rasagiline 1 mg
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