PFS and Huntington’s Connection (CAG repeat)

After reading Axol’s and Awor’s paper on Androgen Deprivation Syndrome yesterday I starting digging around and found a man who has been proposing that environmental pollutants whether that’s heavy metals, pharmaceutical drugs or illegal drugs are the cause of mutagenesis leading to cag repeat disorders and thus the likes of Huntington’s disease.

This was his post: Working on finishing up my complete take on Huntington’s Disease, rather than the short version I’ve shared earlier. It’ll probably be about 100 or so pages when I’m finally done. Planning on using something like this for an introduction.

My position (in a nutshell)

I argue that, contrary to the conventional consensus, Huntington’s Disease is not a genetic condition, but an environmental one, with a genetic component (like most, if not all other diseases) which I argue is the effect of exposure to mutagenic environmental pollutants (like methylmercury), and is, at least in part, a protective adaptation to deal with such problems as manganese pollution exposure and the health complications they lead to, like cancer. I also make the case that the CAG repeat expansion mutation that allegedly causes Huntington’s is neither necessary nor sufficient to cause the phenotype in question and provide convincing evidence that a diagnosis of Huntington’s has been used, consciously or not, to mask i) cases mercury poisoning from industrial pollution (including most recently and obviously among the First Nations Innu in Canada situated along the polluted St. Lawrence River), ii) fungal/mycotoxin complications, and iii) drug induced illness, and that these complications can better explain both the HD phenotype (chorea, Parkinsonism, dementia, etc.), and various bio markers (such as polyglutamine aggregates, gliosis, selenium deficiency, GABA deficiency, and more). My multifactorial causal analysis of the Lake Maracaibo cluster that was used to determine the alleged genetic cause of Huntington’s makes clear that petroleum pollution problems (which mean mercury pollution problems) from the likes of the same Big Oil corporations that have funded this research (and more) are the more probable primary causes. I what follows, I make clear i) how my revisionist hypothesis has far more explanatory and predictive power than the consensus I believe I’ve thoroughly refuted, ii) why my hypothesis, unlike the genetic hypothesis, is not undermined by the existence of numerous geographical clusters that, for any other condition, would be taken as clear evidence of environmental causation (at least by persons not being financed by the relevant polluters), and iii) why my hypothesis, unlike the genetic hypothesis, is not undermined by the recent challenge to the amyloid hypothesis from the antimicrobial and antimetal hypotheses, but is rather strongly supported by such challenges.
I also give credit where credit is do by making clear how my analysis is an extension of Mark Purdey’s work, but also an improvement upon it, mostly due to my adding mercury, fungus, and drug induced diseases to the equation. Purdey claimed that his multifactorial analysis of the Machado Joseph Cluster on Groote Eylandt ought to generalize to related CAG repeat conditions, including Huntington’s, and I believe that my analysis of the Lake Maracaibo cluster is (more or less) what Purdey would have had to say had he gotten around to researching this cluster, and/or the other HD clusters. And based on what I’ve added to the causal equation with the help of Huntington’s Disease, moreover, such an analysis now, I argue, has the resources to cover (at least) all the big neurodegenerative diseases and their corresponding geographical clusters. Which is precisely what I used it to do when I go on to cover the other, lesser known genetic repeat conditions likewise connected with the right kind of pollution problems that Purdey didn’t get around to covering (like Friedrich’s ataxia, and Fragile-X), in addition to a neurodegenerative disease that’s supposedly 100% attributable to trauma: CTE. I’ve also used what I learned from my Huntington’s analysis to shed more light on clusters that Purdey did cover (by discussing the causal relevance of the Kuru cluster having been found by gold miners, for instance). Even if my revisionist analysis isn’t exactly right, or at least complete, I think it’s impossible to deny that i) my contribution has raised important problems that have thus far been unaddressed by those defending the genetic consensus, and ii) however flawed my analysis might be, it’s still far superior to the alternative I expose as based more in eugenicist ideology than science.

“Nonetheless, we have determined that chronic exposure over a three month period to a number of genotoxic agents can alter the rate of triplet repeat expansion in whole populations of mammalian cells. Interestingly, high doses of caffeine increased the rate of expansion by approximately 60%. More importantly, cytosine arabinoside, ethidium bromide, 5-azacytidine and aspirin all significantly reduced the rate of expansion by from 35 to 75%. These data establish that drug induced suppression of somatic expansion is possible.”

Ok so, how to solve it?

Million dollar question

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“Positive Correlation between Androgen Receptor CAG Repeat Length and Metabolic Syndrome in a Korean Male Population”

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For us idiots, is coffee a good thing or a bad thing in this study?

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Indeed, very interesting topic. Shorter CAG = Supersensitive AR. Rapists have short CAG according to one study.
HDAC 3 inhibition suppress CAG expansion.

https://www.nature.com/articles/s41598-017-05125-2