On the off-chance that psychosomatic suggestibility is on this list, I'm not even looking at it.

This is great, check my post history, I've been beating this drum for many years now. hEDS is very very very under-diagnosed and this one simple fact is sufficient to explain a the prevalence of a whole zoo of seemingly unrelated conditions. There is an incentive to keep hEDS as a 'rare' disease as the US has extra grants for disease in this classification and this has put pressure on diagnostic criteria which was made more strict so fewer people would be diagnosed with it.

I'm about to head out for lunch so this will have to be a shorter post but I'll touch on some of the major points.

* The progression of prevalence of hEDS over the years has gone from 1/50K, 1/15k, 1/5k, to 1/500 which is insane. Most people are using values from older studies so they think it is much rarer than it actual is.

* I don't see a strong distinction between hEDS and HSD, diagnosis appears to be mainly a matter of severity but due to that being rather random there isn't a clear distinction.

* The TNXB gene is overlooked because too many people have SNPs here and the assumption of the rarity of hEDS rules it out. It seems that number and type of TNXB SNPs as well as other RCCX genes also govern severity.

* If you look at long covid information the proportion of those who have hEDS/HSD is far higher than it should be. Dr Jessica Eccles has great research on this, I think the obvious explanation here is far more people have hEDS/HSD than have been diagnosed with it, and these conditions create a strong predisposition to ME/CFS/LongCovid.

* Average time to diagnosis is 20 years from the onset of symptoms, which is insane, but it gets worse when you consider that the vast majority with it never get diagnosed, so the average is really never.

I have a rather severe form of this and even I would have a hard time getting diagnosed with hEDS - I look too healthy. I've never been formally diagnosed but have a Whole Genome Sequence with the expected TNXB SNPs. Things that I've tried and worked;

* Low Dose Naltrexone (LDN) is a great start (mentioned here in the pdf)

* Supplemental T3 as sub-clinical hypothyroidism is pretty common

* I think a combination of weak ligands like Modafinil and Amitriptyline can really help with dysautonomia

* I take low dose of semiglutide and this seems to help with the auto-immune aspect

* I take Ipa/ModGRF(no dac), BPC157/TB5, and VIP

* High dose TUDCA and high dose DIM

* Supplemental testosterone

* Zero sugar diet, including no fruit. I basically subsist on kale salads and steak.

This is a stark reminder why you use LaTex or typst with a good template for typesetting your scientific contributions.

Unless you learned basic typography that is.

This eyesore looks like it was done in Word & Co.

What a pity, given what a treasure trove this is.

As someone with a partner who has ADHD I think this should be mandatory reading for any GP.

Extremely important information. Other connective tissue disorders can also present with these findings.

"This resource is intended as an introductory primer for primary care clinicians"

Anybody have a more non-medical-background summary?

I've been learning a lot about this sort of thing. I was diagnosed with ADHD in 2020 or so, and just the past August was also diagnosed with celiac. It seems that there's some pretty strong correlation between the two.

Autism and ADHD are a (deep) habit of the attention.

A habit of moving the attention in a way that is possibly unhealthy, unuseful and probably discordant to what's common and normal.

One solution is to change that habit with drugs or therapy.

Another solution is to gain a greater understanding of your attention. Thus gaining a new freedom to move your attention in whatever way, rather than suffering the governance of habit.

The meditation people (Buddhists etc) study attention. They have some impressive methods and such. It's worth looking.