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Old 02-13-2011, 09:18 AM
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reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
reverett123 reverett123 is offline
In Remembrance
reverett123's Avatar
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
Default Some data

Discussion on this forum and elsewhere indicate that about 50% of us remember constipation as a childhood problem, a rather high number in my opinion. That can be "spun" to support either hypothesis I suppose. But there is no denying that there is a general improvement after a BM.

The recirculation of toxins is an obvious danger, but another is the introduction of partially digested proteins into areas of immuno-surveilence. This can lead to autoimmune problems since the small proteins can lead to cross reactions with our own tissues.

Constipation alone probably isn't enough. However, the addition of bacterial induced inflammation of the GI tract ala H pylori would alter things rapidly as it disrupted the barriers. H pylori protects itself from our stomach acid by a process that produces ammonia. Ammonia is normally cleaned up by the liver but if it gets overloaded then the ammonia moves through the bloodstream and reaches the BBB. Inflammation in this area would allow the breach of the BBB and the passage of the (deadly) ammonia.


Quote:
Originally Posted by johnt View Post
Confidence in faecal transplants would be increased or decreased if the following hypothesis could be proved or disproved.

Hypothesis: rather than Parkinson's causing constipation (as I'd always assumed), it is rather the case, that with the wrong bugs in the gut, Parkinson's and constipation reinforce one another: Parkinson's slows the transit time, leaving longer for toxins to build up, leading to a worsening of the Parkinson's, and so on.

If this hypothesis were correct, we would expect to find that:
- once the body has recovered from the stress of defecation, symptoms would fall to a minimum and then increase progressively until the next defecation. (It could be that the effect of years of damage swamp the short term effects);
- the probability distribution of the time between defecations is U-shaped. (The hypothesis would suggest that you have a period of reduced symptoms when the chances of going again are good, but if this opportunity is missed it gets harder and harder to go, until eventually the issue is forced.)

Has anyone got any data or references?

John
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
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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