[cjbgkagh]

Very much disagree with the implication that helminths will help very much for these conditions. While not a commonly known treatment in the 'medical sphere' it's is very commonly known in the 'patient community spheres' and from the patient run studies it does not appear to have a particularly strong effect. It does appear to help some people so it's hard to rule it out but that could easily be noise. Those who did report a benefit were most often in the less impaired category and those same people tend to benefit from a wide variety of treatments that are generally ineffective on those of use who are more impaired.

This post reads like someone who has just discovered the world of ME/CFS/LongCovid (post viral) /ToxicMold/POTs/SIBO/IBS/Lymes/hEDS/Graves/Hashimotos/MS/Lupus etc. etc. As a lifer I have seen many people enter the space and go through this exact same early stage of discovery.

What I really think it is; it's genetic, various types of generalized anxiety disorders with their associated auto-immune conditions with the most common being Hypermobile Ehlers Danlos. These genetic predispositions are made worse by diet and lifestyles and triggered by all manner of stressors.

On how to treat it, Low Dose Naltrexone is a good step one, then meds for dysautonomia, TUDCA, 3,3′-diindolylmethane (DIM), and then finally I think Low Dose Semaglutide < 0.1mg per week is going to be huge for auto-immune. It's early stages but few things have appeared more promising in the patient community. It worked wonders for me and a few other people I know. Everyone is different but those are in my opinion a good place to for someone starting.

Helminths did not work for me the several times I tried it and have not worked for anyone that I have personally known that has tried it which to date is around ~10pp. But I do believe the people who do say it has worked for them but I don't count them unless I knew them prior due to the issue of selection criteria biases.

[pazimzadeh]

The Th1 program in a T-helper cell suppresses the Th2 response, and vice versa. https://en.wikipedia.org/wiki/T_helper_cell#Th1/Th2_model

Although it's way more complicated than that and there are exceptions, but it's still a real phenomenon.

Community deworming increases Th1 cytokines https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098677/

When you administer helminths to yourself there is no guarantee that they are going to the right spot in your body, etc. which explains why everyone responds differently.

[lav42]

What is it you're suffering from? Do you have references / communities / guides? I have Ulcerative Colitis which I got around 2018 and it seems well managed.

Since my first COVID infection, I ended up with repetitive thoughts, short term memory problems, difficulty focusing, light sensitivity, fatigue ...

It got better but it seems that seasonal allergies re-trigger some kind of cascading inflammation and I've been useless for most of the summer.

Are you talking specifically about long-COVID?

[cjbgkagh]

Mine is ME/CFS from hEDS made worse by the covid vaccine. Patient led 'research' I'm talking about is done off the books in private chat groups / discords / telegram - so nothing is published. That's a double edged sword - but given the slow pace of normal medical research we just couldn't wait. Given that it's grey / black market these groups, the ones that survive, are extremely private.

Those listed conditions are a set of overlapping clusters that have a lot in common. Some of the listed conditions do have distinguishing comorbidities. The things you listed does appear squarely in the shared comorbidities and not in any of the distinguishing comorbidities - so it could be any number of things. The Ulcerative Colitis does increases the likelihood that it's hEDS which is already the highest likely predisposition @ ~2% of general population and higher for the HN population and even higher again for physics people (not the published figures of 1/50K, 1/15K, or the 1/500 which I consider to be incorrect due to the incorrect assumptions for disease state thresholds in the diagnostic tests).

Probably the best lens to look at it would be through the lens of dysautonomia which is a balance of a not well understood by the vast majority of doctors yet reasonably well understood by a few doctors - enough to be able to find decent information in medical research. My preferred meds for treatment of dysautonomia are modafinil and amitriptyline and these meds also act as immunomodulators - the same thing the helminths are supposed to help with. Modafinil can exacerbate gastro issues so in my view people who have those issues should focus on amitriptyline first (at the sleep aid doses not the depression doses). And googling it now it does appear that amitriptyline is indeed a known treatment for Ulcerative Colitis.

[lav42]

Curious to know the origin of your likelihood calculation (HN & Physics).

Also very funny you inspect my account to figure out I'm a physicist.

[cjbgkagh]

That's how I get my data, well at least substantively check some of my data. Behavioral analytics a.k.a big anecdata. With great care and restraint it is possible to extract useful information from a large amount of biased sources - just can't publish it unless you want to spend the rest of your life arguing with people who argue for a living and do little else (academics).

With enough data it's possible to disambiguate between genetically linked behaviors and learned behaviors because of the different diffuse patterns through disparate populations. The summary is that behavior and intelligence is absolutely dominated by genes, there is really only a 13% residual - so on a nature vs nurture spectrum the nurture is less than 13%.

The stronger the selection criteria bias on intelligence the more likely a RCCX gene variant (SNPs) will be selected, specifically TNXB (burnout / ME/CFS), C4 (schizophrenia), and CYP21A2 (generalized anxiety disorder).

You may wonder why this doesn't come up in GWAS studies - usually there is an assumption of independence of SNPs due to the idea that most SNPs are very old and genetic drift has been sufficient to provide this independence. Since these individual SNPs are so behaviorally impactful there a strong sexual selection bias that takes place so those assumptions don't hold and thus the math is bunk. I could spend forever talking about the incompetence of medical research.

Dr Jessica Eccles is probably doing the best research where she talks about the shocking 'overrepresentation' of Generalized Hypermobility Disorders (GHD) in the Long Covid populations. In my view the only difference between GHD and hEDS is the number and severity of TNXB SNPs, so while 2% of the population are impacted most of those are only mildly impacted. The co-occurrence of multiple TNXB SNPs is much higher random chance - again from the aforementioned sexual selection biases. In general researchers into such conditions assume TNXB SNPs are far too common to cause such a rare disease, the thing is that it's not a rare disease - just rarely diagnosed and surfaces in a variety of complex ways that look completely different to the untrained eye.

You can get a Deep Whole Genome Sequence for ~ $280 from dantelabs and then you'll know for sure.

[jph00]

But the article isn’t implying that. In fact it explicitly says that helminths can be dangerous.