(It doesn't mean that it is impossible to have chronic kidney disease if you have PD, though.)
Why is this? Maybe it is due to the lower uric acid levels in people with PD, or maybe it has something to to with differences in alpha-synuclein, which is expressed in the kidneys. Perhaps a-syn has something to do with ENaC, which is involved in fibrosis.
Intriguingly, PD seems to decouple the relationship between diabetes and CKD.
Active vitamin D (calcitriol) and klotho are lower in PD and they are also produced both in the kidneys and in the brain.
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Was the the Mexico City study flawed - maybe just too small? There's another study from Europe that has the adjusted odds ratio for PD in CKD to be 0.80 - which means lower risk??; I'm not sure if I am interpreting this correctly:
The Mexico City study findings, if true, are really interesting. It looks like has not been published in a journal, so I will just give up on it for now.
Mmm articles I’ve been reading on mycotoxins particularly ochratoxin says they it is often elevated in pwp. And when it is excreted it is commonly through the kidneys which is toxic to the kidneys. So does that mean that it is higher In pwp because the body accumulates it rather than excreting it, sparing the kidneys?? I have No scientific basis for this, just wondering.
I think PwP may just have higher exposure levels. Studies on mycotoxin exposure in people measure urine metabolites, so if there are epidemiological studies on it (Mischley may have done one?) linking PD to mycotoxin exposure levels then I expect they used urine metabolites.
There is an interesting study showing that a-syn is protective against kidney fibrosis:
a-syn interacts directly with the cell cytoskeleton, and apparently not via ENaC. However, since ENaC interacts bidirectionally with the cytoskeleton, then to me that means that a-syn can affect ENaC - which is very interesting and why the Mexico City study caught my attention in the first place. I suspect that susceptibility to PD and similar illnesses is related to differences in ion channel function/expression.
This brings up the question of whether a-syn production is generally increased in PD (it is, of course, in cases caused by SNCA duplication or triplication) and whether it increases along with progression. These seem reasonable questions to ask since sometimes if a protein becomes non-functional feedbacks are triggered that increase its production to try to make up for the loss of function.
So what do we know about a-syn production levels in PD (not associated with SNCA duplication or triplication)? It is actually quite difficult to search for this in the literature. Here's what a review from 2012 has to say:
"A comprehensive study of multiple brain areas showed that membrane-associated monomeric α-synuclein levels were only modestly increased in the substantia nigra, and not in other brain regions, of PD patients compared to controls; even so, the levels in some PD cases were within the spectrum of control values. In contrast, in MSA, the membrane-associated α-synuclein increase was robust in vulnerable brain regions (Tong et al. 2010). It may of course be that neurons with the highest expression levels of α-synuclein are most vulnerable and succumb early in the disease process, giving their place to glia, thus confounding the results. To partly circumvent this issue, Gründemann et al. (2008) performed laser-capture microdissection studies, and reported a considerable increase of SNCA expression in surviving nigral neurons derived from PD brains compared with controls. However, this increase did not appear to be specific for SNCA (Gründemann et al. 2008). Therefore, the issue is still open." [as of 2012]
And of course, these studies all have to do with a-syn in the brain, not the kidneys.
Hi yes, Laurie has looked into it. I was wondering as hubby has just had the urine test and has high levels so we were discussing it on another thread.
Hi, hubby had a urine mycotoxin test through a naturopath in NZ. It showed high levels of ochratoxin. I had mine tested too as a precaution and mine was even worse! I struggled to find where it was coming from. Maybe coffee, nuts, dried fruit? We eat organic and I think the lack of pesticides may mean mould grows more easily on these. I tried to get info from the government food health agency but no help there or any apparent concern. The GP just looked blank. All the naturopath could offer him was to drink a chamomile tincture as it apparently can cause liver or kidney? damage as it passes through . I can’t see the test on their webpage now but this was the one he hadgreatplainslaboratory.com/g...
which removes contaminants. He took this for 3 months and the start of last year. We haven’t tested again as it was so expensive and to be honest no one seemed to be really able to tell us what to do anyway about high levels.
After the toxaprevent he did go on to become better and better and has had a really good 6 months. Maybe coincidence as he was on different supplements from then too and red light therapy.
One other possible source could be our firewood which I usually handle or gardening which I do which might explain why mine is higher. We don’t have water damage but have done renovations in the past on old building which had some mould. This winter may-July we used electrical heating instead of a fire just to limit mould in the house. That might have helped him mend and eliminate it too. Normally every May he starts deteriorating but this year he got better and better over winter.
From what little I've read, organic actually tends to have lower mycotoxin levels than conventional - maybe because they are more stressed than conventional and produce more defense compounds (phytoalexins).
Great that your husband is doing better now.
Toxaprevent seems like it could help pretty much anyone, if it actually does what it says. Do you know what the ingredients are?
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