I have never tried to address the cause of Parkinson’s disease.  I haven’t done so because that is not the purpose of my personal blog, nor do I want to bore anybody with elaborate or crazy theories.  I am also not a doctor, nor scientist.  Furthermore, as those of you who know me by now are aware, I also am not affiliated with any organization, nor do I seek recognition, financial gain, and also don’t and have never peddled any s0-called remedies, elixirs, etc.  So, in this ONE blog post, I am going to go on a wild tangent – just for today.  I am going to put forth an interesting idea.

It is not a new concept to think of Parkinson’s as starting in the gut.  It is also not new to think of it as a reaction to poisons in some cases.

However, a new hypothesis that I have arrived at, is the following:

What if it was continually fed? Not from the brain, nor “starting” in the gut as most newer researchers presume, but instead the degeneration in the brain is continually fed from by the brain attacking the body, in a process that begins similar to an allergic reaction or autoimmune system malfunction.  Perhaps  ingested spores (mycotoxins) and other neurotoxins, high levels of stress, and other factors initiate the response and attack.

What if treating the brain after this response has been initiated, was the equivalent to treating a forest fire by adding more firefighters, more hoses, or spraying water on the trees – meanwhile, the actual flamethrower was outside the forest?

What if some people’s genetic mutations combined with environmental assaults, combine to create a disruption in the ability for our brain at a micro-level to convert amino chain proteins into dopamine or worse, to attack brain cells or abandon a process of neuroprotection?

If you are bored or think I am way out of line, then stop reading this post now.

For a more scientific way of stating the above:

I am wondering if maybe a genetic predisposition or mutation combined with mycotoxin (fungal/spore – such as small amounts in grains and foods stored in moist environments) or cytotoxins could be enough to create continuous poisoning – and perpetually add to accumulation of neurotoxins in the body either from damaged cells or lack of the brain being able to “clean” micro-toxins”. Maybe there is even an additional interplay between toxins used to treat or fertilize our crops, such as glyphosate contamination interacting with these mycotoxins ingested from spores (from grains, etc.) which could also create a self-perpetuating cycle of continually causing tyrosine hydroxyls disruption after a failed brain response to stop these, especially mitigated by these genetic mutations.

In either case, my hypothesis presents a cause of such neurodegeneration originating from an interplay between environmental assaults and either a perpetual neurotoxic accumulation, or continuously aggravated autoimmune response (or both) resulting from these neurotoxins combined with a genetic predisposition or mutation, such as: an altered DAT system, mutations involving protein-kinase conversions, mutations preventing neurotoxins from creating oxidative stress (disrupting amino acid conversion to neurochemical messengers), and mutations that would allow the accumulative buildup of toxins (such as a MTHFR mutation: that responds to products enriched by man-made folic acid being stored as a neurotoxin, instead of proper methylation conversion).

These individual variations in genetic combinations and reactions to neurotoxins could promote and explain why there may be different forms of the same disease, with commonality in clusters of symptoms being the end result – (i.e. oxidative stress, alpha-synuclein modification and then resulting neurodegeneration as in the case of Parkinson’s disease).  As suspected by some, there may be different manifestations of diseases like Parkinson’s, autism, multiple sclerosis, etc.  In applying this to Parkinson’s disease, this hypothesis, if someday shown to be correct, would in essence make Parkinson’s a disease that would be akin to both a chronic toxic poisoning, an autoimmune type reaction, and possibly a malignant process due to the buildup of toxins causing disruption or inhibition or further damages and other mutations in cell replication. Therefore, the immune system may then attack the brain cell, thus seeing it as being “hostile” such as an invading toxin.

If this hypothesis was found to be true, in practicality, I am speaking about changes on a very micro-level.  So cutting out gluten from the diet, or eating organic foods, would not be a curative solution, given factors such as already established activating events such as micro-contamination from dust, crumbs and the potential for such from the liquids we drink being contaminated.  Perhaps future medications could target neurotoxic build-up, ease methylation conversion, or some sort of future potent antioxidant, or even a vaccine, could alleviate this neurodegenerative process.This hypothesis could have some evidence if we found that in certain geographical areas with people with common ancestry and certain genetic mutations, and who ate and drank from the same food-sources, would then have a strong prevalence of having Parkinson’s disease.  Guess what? I have read evidence for that.  Other bits of information to support this hypothesis would be studies and indicators of immune responses that differ in those with Parkinson’s disease – and there is evidence being collected in this area as well.

I started sharing this hypothesis with “leading scientist” at places who are supposed to be on the cutting edge of finding a cure, only to find that most of these people just review academic experimental studies and approve grants.  I then talked to chairs who head labs and studies at some major universities.  Some asked me who was funding me, what my credentials were, and seemed dismissive when I revealed that I was just a guy with Parkinson’s who was interested in just putting some ideas out there.  Some were interested and had similar conclusions and were sparked with a “maybe this guy may have done his homework” kind of response.  I have even decided to be an anonymous “X-factor” and just put forth my ideas to throw some crumbs (pardon the pun) toward some researchers.

The ramifications if this was even close to being correct would be that we are just throwing small buckets on a fire (by treating the brain by trying to keep up with the demand for dopamine and regulate other neurochemicals) with our targeting the brain solely being misdirected to the wrong place.  We are in exciting times as now scientists are looking at many different aspects that could be contributors (such as prions, TAU, etc.)

Once again, I admit, I may be way off base and totally wrong, and that is okay.  Again, I am not a researcher, nor do I have any ties to any pharmaceutical or financial interest company. I am just a guy with Parkinson’s who had to quit being a psychotherapist because of my illness. I just want to put this out there on the wild chance that I can try to help find something that may have been overlooked about PD.