An export of a mastodon thread that I wrote to complain about the lack of control surfaces to make the interface more accessible to me.

Original here:

The things that make a website accessible to me are simple design. Low distractions from the task at hand, low visual noise and an interface/workflow that can be easily modeled in my head.

Cluttered options, high contrast text and URLs, and things that make websites accessible to vision impaired people end up actually hindering me.

and then you get people yelling about how complicated settings makes a website not accessible because it is confusing and creates barriers.

Makes me angry.

Arguing that customization is a barrier "its too technical" makes me angry. That same way of thinking is why we see games that don't let you change keybinds, or resolution.

It makes me frustrated; I can see both points of view as being valid. Opening up a panel and seeing a complicated keybinds system is inherently less accessible...

Unless you need access to those features.

Accessibility is relative. At some point customization is inherently a technical feature.

A user interface is exactly that, an interface between the computer system and the user in the chair. At a fundamental level, to make an accessible interface is to make something customizable. The interface needs to fit the user's needs.

You get weird problems where mandated accessibility features conflict. A choice has to be made.

But there is an inherent complexity to making something customization, which is itself an accessibility barrier to some.

As an example. I have taken care of my disabled mother for a great deal of time in my life. She's physically disabled, and her apartment is handicap accessible.

On my dad's side of the family, everyone is tall. To make housing accessible to them, they get customized counters that are taller. Literally hitting our heads on door frames so we get taller doors.

But everything in my mom's apartment is short. It literally hurt me to clean her house for her. A trade off.

Some stuff was easier for her in this apartment. She can't do stairs well, and a lot of the features of the place were helpful. But she wasn't wheelchair bound so other parts were harder.

Both me and her have cognitive issues that make it hard to plan and organize. The wheelchair accessible floor plan meant everything was cluttered because there weren't enough closets and the ones that were had oddly shaped shelves.

This all amplified the difficulty of keeping things clean.

What we needed was a space that we could customize for her needs. But customize-ability complicates things. It literally adds cognitive or physical load.

Having adjustable tables, Re-arrange-able shelves, and height adjustable furniture would have been a godsend. But those things have a cost too.

They're more expensive, and you have to learn how to use them. Flexibility of furniture also makes things weaker (bad for overweight people), or significantly heavier (bad good for weaker people).

With physical things, to make something customizable, you have to make the underlying hardware visible. Being able to unscrew and reconstruct the furniture to fit you better also means your furniture is going to have bolts and screws to snag yourself on. There is going to be visual noise from it, and parts of the structure may pinch you if you aren't careful. Its going to be ugly.

I want a social media platform that is ugly. Something with visible code I can reach out and tweak. Sure, it will be hard to use if you can't write code, but something like that would be easy for me customize and tweak for those who need it.

I can make my interface work for me - low clutter and low contrast. But also make it high contrast and easy to use for my blind grandma, and change the button size for my mom's clumsy hands.

But then you get people yelling about how complicated settings makes a website not accessible because it is confusing and creates barriers for people who can't.

You get weird problems where mandated accessibility features conflict. A choice has to be made. Makes me angry.

We can't just wish away the nature of furniture. Someone's gotta build it. Accessible to customize means more sharp edges and more effort to streamline. Or more complex and heavyweight.

You can make customization easier, but it's going make the product less simple.

You can simplify something, but this also means more work to customize.

More complex software is harder to mange/ends up costing more to run.

You can make it more accessible, but then you have to ask "to whom?"

Makes me angry.

Modifying your house so the dog can open doors for you, and other ways that those with disabilities cope.

This is fucking awesome.

"Much of recruitment is now online; the problem is that inaccessible websites and online application systems remain a big barrier for disabled people looking for a job. Over 90% of websites, for example, don’t even meet single-A compliance with the WCAG (Web Content Accessibility Guidelines) set by the World Wide Web consortium (W3C), whereas the legal minimum is AA (a higher standard than single A and lower than top compliance level AAA)."

Lack of Control

[The L.A.B.]

Living Area Blueprint

The Praetor Labs' Developer House Initiative

What is [The L.A.B.] ?

A group name and banner for the Praetor Labs' Developer House and associated projects and initiatives.

A ‘network node’ that connects to other nodes in real space and globally. All nodes, as they grow and are added to by other nodes, form a growing decentralized community.

At Praetor Labs, you sleep in the LAB. You eat in the LAB. You play in the LAB. The LAB is your home.

As a Living Area.

We want to live with cool people. But just being around cool people is not enough.

We want to create a culture of creativity and projects. A place that encourages serendipitous idea sharing, and an environment that facilitates getting shit done. To do this we need people of many disciplines and backgrounds: Art, Science, Computers, Electronics, Design, Writing, Film, etc.  

That is, we need thoseingenuitive hackers and makerswho just love to create. Get enough of these people together, and be generally awesome. A community of awesome.

Mix in a great big dose of FILDI because we are all a little bit crazy.

As a Culture Hack.

Our core values should be to create, educate, and entertain.  We want to develop a culture that inspires the creative and industrious part of people, and helps others do the same.

Long term goals include the development of a social media outlet and platform to share our ideas and attract other followers to projects for fundraising, ideas, and general assistance. And the creation of resources that help others do the the same.  

But this doesn’t mean we spam ourselves all over the internet. The idea is that the stuff we create will sell itself, and those interested in us will find their way finding out more of what we do.

As a Blueprint.

The Lab is intended to be an "Open Source Culture Platform".  To create what the global village construction set is doing for agriculture, only for creative community building.  To develop systems that augment and evolve the already awesome maker-spaces, and create developer flats and maker-houses. A blueprint for hotbeds of creativity.

The house is a potential bootstrapping framework for the creation of an open source democracy. The idea will be to develop an adaptive and grass-root style fluid hierarchy.  The hope is to inspire autonomous teams of people all working toward shared goals that improve our communities and environments. Hinging on ideas behind distributed command and control structuresand the passion inspiring aspects of pull, we hope to allow for individual creativity but with a nod toward community driven goals.

Basically, create tools and processes that help groups of small and agile development teams meet real world demands and turn on a dime as opportunities occur. Being a living area, the focus will be on local communities and neighborhoods. On the larger front, Hierarchies will form and deform as different groups latch on to various goals. You vote by what you work on.

Apply agile software development ideas and ideals to real world projects.  [The L.A.B.] is our test bed to find out what works, doesn’t work, and what we need to make it work.

As a Bootstrapped ‘Business’.

Taking ideas from The Lean Startup we want to turn our hobbies and our passions into things that support themselves. We don’t want to worry about how they affect our day jobs, nor do we want them to take up all our time.

What good is a community that is not self-sustaining?  If the community cannot exist without outside funding, it is neither robust, nor resilient.  This does not mean we all need to be millionaires, but it would be nice to create something that is profitable.  This means we’ve done something we like doing, and will be getting paid to keep doing it.  A side goal will be to minimize the startup footprint and costs so that others can create their own community of awesome.

Ideally our house will eventually become a Vermont Low-Profit LLC organization (L3C) so that we can market products and make money as a ‘business’ to further our cause(s). It should be a low-profit in the sense that our goal should not be "return on investment", but rather a focus on "return on community".

Any excessive resources we gain should be funneled back to the house’s projects and initiatives, with an ever widening goal of improving other people’s lives and improving our own efficiency at doing so. We want to give back to the community, and become part of it.

Our vision is to become one of the few companies that are: Bootstrapped, Profitable, & Proud.  

Will we make stuff that helps people be frugal?  Will we help them live well? Will we make something to learn better? Create something to mow their lawn?  Don’t know. That is part the the fun.

TL;DR. (Too Long; Didn’t Read)

If nothing else, [The L.A.B.] will be a great self-governed dormitory style house where we can make cool shit and do cool stuff with cool people.

TLDR; throw a whole bunch of smart, creative, and ambitious people together, mix in the right set of ideas, tools, and space to work, and see what happens.

The [L.A.B.]

Hey, Sorry to hear you're having trouble.

I don't really do consulting work. I am not a doctor and my life is too chaotic to be reliable here. Tho it is kind of you to offer.

I tend to share what I have done for my own health, and link to studies I've read on topics / redirect to other people and resources that might help. I don't really offer consulting or medical advice. More seeking other people who want to share knowlege and help figure out what is wrong with us. I'm mostly doing what I do to work on my own health issues, so I don't really expect payment or provide services per se.

I enjoy sharing what I learn about things, however. My tweets are searchable and I keep an collection ( ) as an attempt to communicate, albeit done in a very strange way.

I would love to talk to you about what you've been doing so far. I do best with that mode of discussion because it triggers my memories for tweets and topics of mine that I've researched. Talking with other people about their health explorations helps me learn about my own challenges, and asking/answering questions helps me linearize my own chaotic headspace. So even if I was acting as a consultant, I would feel bad charging money because I get just as much value out of this as you would.

I tend to recommend people move to a more secure platform to discuss health stuff as I don't personally trust DMs to not be hacked or snooped on. I have a signal and a keybase, and recently set up a telegram that I believe can do encrypted chats (Tho it's harder for me to use that as it won't work encrypted from the desktop client).

I used to work in information technology support so know a bit about medical information security, so it makes me uneasy to have other people talk about their health issues here.

I am not a doctor. I do not charge for …

Reading Fast and Neurodiversity

(also on @UltimApe's Garden )

How do you read so fast? Any tips? I used to get a measure and I'm still only at 200wpm and am trying to figure out why.

Also, do u think there is any real benefit to the flashing word speed reader apps? ( "Rapid serial visual presentation")

I like them. I can read about 1200 wpm with those RSVP things. Faster if my monitor's refresh rate can handle it. Literally doubles my normal reading speed.

It loses the spatial aspect of the page tho, so it doesn't work well for stuff that requires going back and forth between things (like science pubs).

It depends a lot on your ability track eyes across the page and general issues with motor control. You also can get a lot faster if the thing takes into account the eye position like how spritz does. There was an open source alternative to this that was nice.

Reading thru my notes, it seems I was using "squirt" for a while to train. I also collected a bunch of notes on speed reading

IMHO, a good one would also be watching your eyes for blinking,and none of the existing software does that well. The pacing also often doesn't adapt to word complexity at all and treats each word the same. That might not be ideal for reading comprehension. For actually reading, It seems more like a novelty than anything.

If you struggle with reading issues, I recommend playing around with something like a kindle. They give pretty good controls for line-width / gutter height and text size that helped my ex read a lot faster than she did with normal books. She had pretty bad dyslexia.

I've been looking for a plugin for browser that helps with this, but websites are all too unique to help. When my eyes were having trouble I just copied text out into word/open office and changed the line spacing instead.

There are ways to mess with this via CSS, but without some kind of plugin to automate it, it's usually not worth it unless you have an entire book to read.

The CSS property is "line-height" you can see how it changes in this demo (click the boxes on the left to select and the text should adapt)

It gives a sort of natural ruler effect to help the eye move between lines.

How do you train yourself to read faster? I've been using a tool on the ipad that has a flashing text and a line-highlight. What one is better?

Most optimizations people have for speed reading are about eye scanning. Typically the less your eye jumps around and back-tracks, the faster you can read. Sometimes problems here are due to motor control issues in the brain.

Those flashing text ones are nifty because they literally remove the need to move the eye.

Thinking about it as training exercises, you can train your eye with spritz etc. to lock onto the best part of a word for reading, and then use line spacing and other tools to help get your eye to flow in straight lines. Between both of them, your brain can rewire to be better at it.

Over time your brain learns to read entire words at a "glance". and then you can start expanding how many words you read at once by training more effective use of your eye's center vision area where lines are most acute.

So I think of those flashing word things as a tool to train a specific kind of pattern recognition but not necessarily good for all the time stuff.

The highlight mode there looks like a way to train your eyes to move across the page. I'd say go only as fast as you can comprehend things with it and then push yourself a bit in bursts. If it is indeed a learning phenomena, it might be like how sometimes your brain needs to sleep to integrate the learning too.

Maybe suggest alternating between normal, highlight, and flash? like a different mode each day. Flash day is good for word shape recognition. Highlight day is good for eye movement consistency, and then regular day is to allow you to integrate the two skills without the aids and test to see if you are improving.

I think of it like how athletes will exercise individual muscles and for a while and then also spend some time doing their sport in practice. What matters is how good you get at regular reading, so don't worry if your flash or highlight reading isn't improving.

I think the trick is to figure out which "muscles" needs to be exercised. I couldn't tell you how to figure that out tho. I believe you need to play around with that on your own and experiment.

Something I remember growing up that may have been a big help for my reading was having a parent read to me while moving their finger along the page along with the words as they went. It seems to be a way to train the eye without depending as much on reading comprehension because their spoken word was compensating for needing to read.

So might recommend seeing if you can get it to speak to you? or find another app that can do word highlight-as-it-reads.

Do you ever have trouble reading

When my immune system isn't doing well, I start hallucinating words. And I have to make sure lines of text aren't too long otherwise I end up re-reading the same line over and over.

My big problem is with my own writing. I don't notice duplicated words words or speeling mistaks. I remember what I meant to write, so when I read thru again to check, its like my brain just edits out the mistakes.

You don't really seem to make many mistakes

I've been feeling really good today! I also seem to be thinking faster than usual too. I've been doing better since doing the dog trial. I don't seem to encounter brain fog as much.

Oh, that might mean my glasses being messed up could be working against me? I also have a slight lazy eye.

Strong feelings: don't train yourself to speed read with distorted glasses. That's gonna be training the eye to move weird.

Def look at fixing glasses or any kind of visual distortion first before you go about training anything.

I imagine part of the challenge with speed reading is adapting to different peoples needs. Hard to say really what would be good, and we may need to customize things to the person.

Def think getting it so you're not having fatigue from glasses distortions would be good to explore.

I was looking into these "Hillary Clinton's special eyeglasses to stop 'double vision'" a while back. Apparently there are some strange eye distortion glasses that have helped autistic kids too. The mental fatigue thing with vision problems is pretty real.

I don't know how to fix the lazy eye thing yet that some people have. I know that the lateral eye function thing shows up in both autism and Multiple Sclerosis. My left eye has really weird vision compared to my right. I actually have two different color shades.

Exercise and training can help, but I suspect there is more going on with coordination between things like ciliary muscles (iris) and the socket moving muscles and how the brain learns to move them.

It autistic types, it seems the brain itself literally can be lopsided a bit, with the eye being strange as a result.

Brains of autistic people show unusual left-right symmetry

I suspect it's related to epigenetic expression factors tied to neurodegenerative disorders. This is especially interesting to me as this phenomena shows up in Multiple Sclerosis too. There are some fascinating parallels between the two disorders that people seem to be overlooking (hah).

Tendon development and gene expression factors show up during gestation at the same time as the brain forms. It was actually related to one of my first hunches around genetics. The COMT gene plays a role here, but there is a lot more going on. COMT gene influences TMJ and that is another strange thing that shows up more often than not in my forays into research.

I do think you can perhaps change the expression thru some kind of physical therapy and diet, but what that is I can't tell you.

Genetic, epigenetic, and mechanistic studies of temporomandibular disorders and overlapping pain conditions

All this stuff ties to brain development factors and eye factors. so the hunch about TMJ is good. I just can't say how to actually address it.

I can see better in my right ----> eye

What I do know is that major depression also has asymmetry in how the brain shrinks. So presumably things that improve depression would also help the brain here? If that factor is some how reversible, it may be tied to remyelinating of the brain in Multiple Sclerosis, and so may also be tied to eye function in the same way. But this is more just a hunch.

Something that has been on my mind lately are feedback loops. How a small bias ends up building up due to behavior cause more of something to express.

Like a penchant for sweet flavors / pica in autistics can lead to autistic types eating lead paint (lead acetate taste sweet), which can lead to more autistic behaviors. That kind of thing can become self reinforcing because it amplifies each other.

For me and couple people in my family, sucking my thumb on one side may have enhanced a preexisting bias, maybe autoimmune or a viral infection, or some of other factor.

Nobody is perfectly symmetrical IIRC, so its fascinating to think that maybe what occurs here is a good feature that ends up being on the extreme end.

There has been studies on chickens showing that they actually need to have a slight asymmetry because otherwise they get too distracted by stimulus because both eyes compete over the attention.

In this context, Feedback loops tend to have dampening effects to prevent it from hitting extremes. If it is epigenetic factors and stuff like thumb sucking drives it, what would be dampening it, I wonder?

I personally think this kind of thing is awesome. My bias is to reframe this stuff as super-powers in disguise. If we can find out more about this space, we may even be able to find alternate pathways that would compensate for the negative aspects of it.

A more direct example for me is how the liver processes serotonin. I found out that my liver is on a hair pin trigger here. There's a sort of chemical switch that senses how much is in the blood, and when it fires off the liver shifts into metabolizing it away. Mine is set very low from what I understand of the genetics. So instead of depending on my body to maintain serotonin, I figured that I could help my depression and gut health by focusing on more rapid production of it.

Too much serotonin is bad, but so is too little, so homeostatic regulation helps the body keep within an ideal. Its like shivering when you are cold or sweating when you are hot. People don't typically sweat all the time, or shiver all the time.

But I actually do sweat a lot more than most, which is probably an adaptation tied to serotonin processes (serotonin controls body temperature). That and just problems with insulin regulation tied to the M.S.

So you see it as a superpower because it gives you more insight into what is going on in your body than other people typically have?

The autism bits? Yeah. But more than this, I think part of it literally is a skill that gives me super powers. I can't keep track of time or know what day it is, or even remember faces or names. But my spatial memory is extremely over developed. And to compensate for my other memory issues I've leaned into using it. So like sucking the thumb, it's changed how my brain was trained and grew.

I can't prove this idea until I can get a brain scan.

First there is just the deficit, the negative trait. But then learning to compensate for it kicks in. Like recognizing faces. I can do that better now after learning I can retrain what I have to keep track of it better. I found I can encode emotions in my spatial memory. So I encode faces by the way people make me feel looking at them. Synesthesia like.

An example of the kind of encoding I can do now: A nose makes me happy sometimes. It reminds me of ex wife's, or a childhood friend. A chin and lips can trigger laughter (a friend I remember from it is funny). And then eyes are and hair can trigger annoyance (Say from my sister annoying me when I was young).

Breaking it down like that lets me store it more effectively.

Most of it this requires focus and attention to do, and my diet / gut problems challenge my ability to keep this associative-memory active all the time.

High upkeep, costly to do. That fatigue thing from the glasses would make it impossible for me to do, for example. The super spatial memory thing is impossible when I'm tired. It ends up a jumbled mess.

It's really all about compensating. The weaknesses are still there, they just get accounted for. It's a weakness that I can predict and account for now somewhat.

Like, I can predict that if you pop up in my memory, I might call you "john from twitter". I know my brain will transpose the memory of my friend's name with yours. So in my notes I'll put "john not john" as a short hand for when I need help to get the right memory.

In this case, the compensation is a speed/accuracy tradeoff. Wandering thru my notes take a while sometimes, especially when I'm fatigued.

when did you start developing these memory devices? What age?

1998-1999? So about 11yo. I was forgetting to do homework and realized I needed a way to remember dates better. Started organizing my trapper-keeper spatially. Learned how librarians organized books in space and it mingled with some stuff I was learning about computer algorithms about compression.

I have a bookmark to Wolfram Alpha to tell me how old I am, cuz I always forget, lol. says I'm 34. I thought I was 36 lmao

I've always had the spatial memory weirdness. It seems sometimes common among autistics. It can get pretty extreme.

Nonverbal autistic boy, 8, learns to communicate with mum through Google Maps

I've only had issues with processing speed, not that kind of thing. Is that normal for autistics?

I've always been particularly unique so I can't really say what normal is. The sleep problems / non-24-hour syndrome seems rare even among autistics.

There's this added annoyance about how autism as a label is a sort of black box diagnostic of traits. it doesn't really concern it self with all of them. There may be a subtype thing going on that we just don't have the data to figure out.

My processing speed changes quite drastically too. some studies on brain scanning of autistics suggested that brain activity fluctuates quite a bit thru the day. This stuff is only really now happening because before the brain scanning tech wasn't functionally wearable whiled doing basic tasks.

If I eat things that causes my gf's insulin to spike (she's type 2 diabetic) I noticed I get dumb after a few days on it. It's like my brain starts starving itself or something. Something weird going on there, cuz I don't measure as having diabetes symptoms.

Whenever I find something that helps me think it always interacts with TRPV1 or TPRM8. hot and cold sensory neurons that have an impact on smooth muscle tissue.

Dumb stuff like making sure I don't have to poop, or taking a hot shower. It all seems to come down to blood vessel regulation. Smooth muscle tissue is the kind of muscles that impact blood flow in the brain.

You have M.S. right so does that make you constipated hence the dog shit. Do stimulants affect you?

I think it's Crohn's / IBD or IBS related. Gut inflammation => constipation => immune flair up => M.S. activation.

I haven't had Crohn's symptoms since a week after starting the dog shit :o

The insulin seems to be tied to M.S. stuff too. Insulin problems makes people cold. I was having really weird cold hands and feet a couple years ago until I figured that out. Switching to keto made a huge difference for me, but it wasn't a panacea. Cold feet runs in my family and it's been with me since puberty.

Do you mean the Raynaud's phenomenon?

yeah, tho it wasn't as extreme as people show online. I don't have the full cohort of genetics there. Never went completely 'black'. but def would lose color and less blood flow.

My whole hands and feet turned white, it never had the distinct lines like they show.

Raynaud’s phenomenon (examples)

What genes should I look at?

Raynaud's isn't well understood, so there is strange overlap with other autoimmune diseases.

For example, most of these have been at least partially implicated as contributing to it. These are all the Crohn's risk genes I have.

rs7574865 rs1050152 rs2066847 rs2201841 rs7807268 rs3814570 rs12037606 rs6601764 rs11209026

But there are also ones in rheumatoid arthritis and M.S. that show up. They tend to also overlap with Sjogren's syndrome and lupus.

I got a smattering of them all, tho I bias toward RA and Sjogren's on top of the obvious M.S. and Crohn's ones.

I think this site explores the associations a bit but it's been a while since I was digging in so the memories aren't fresh.

Cuz they don't understand specifically what causes Raynaud's, the genes aren't very specific. It may be viral / autoimmune caused, so it may explain why genetics aren't definitive.

An Autoimmune Basis for Raynaud’s Phenomenon: Murine Model and Human Disease

My big hunch is it's not predominately genetic, but Gene expression / epigenetic, and everyone looking for genes have been searching for the wrong answers.

Lots of risk factors for autism involve diabetes and infection in mother. Both of these impact gene expression. Throw in gut bacteria's impact on this space, and weird findings about famines during pregnancy causing autism/schizophrenia risk in children...

Easy to extend this model of thinking to other poorly understood disorders like Raynaud's. The thing we are overlooking is that both diet and gut microbiota are past down just as much as genes.

Genes create the environment

I think gut and diet can compensate for so much. If I eat lactobacillus lactis, it literally doesn't matter that I have lactose intolerance genes as the milk stops causing me problems.

And fermenting stuff externally to get nutrients the body doesn't process well is another thing that humans have done for at least 40,000 years.

As far as I can tell we've co-evolved with this kind of thing going on. Just as much as how insects co-evolve with mushrooms and flowers to provide food and medicine.

Western science seems to have hyper-fixated on genetics as the only way that Darwin's decent with modification can take place. As an institution it completely ignores any other mechanism that could impact this space.

It's myopic.

We got studies like this one:

We then created a manipulated microbial community with titrated doses of Collinsella, demonstrating that manipulation of the composition of the microbiome under both natural and controlled conditions leads to distinct and predictable gene expression profiles in host cells. Taken together, our results suggest that specific microbes play an important role in regulating expression of individual host genes involved in human complex traits.
Gut Microbiota Has a Widespread and Modifiable Effect on Host Gene Regulation

But everyone that is in the field ignores it or doesn't get the implications of how far reaching this is. We're raised from childhood to have one particular view on how evolution happens and its always "Gene this, gene that".

It is in the end, but its interactions between genetics and inputs at a higher level. We consider organisms as individuals. But evolution also acts on groups too. Throw in horizonal gene transfer between bacteria and viral effects and most of the modern theories on genetic evolution suddenly seem completely wrong in how they are applied.

Sorry, this is me being a crank :)

I think I may be fundamentally confused about what a gene is?

So typically SNPs like you'd see in promethease are shared as genes. Larger units that consist of multiple Single Nucleotide Pairs. Genes tend to be remixed thru sexual selection as entire units, all the SNPs at once.

Mutations are quite rare in this process. And most of the time they are benign. Even when they do mutate something, we also often have multiple copies so if one copy is making a bad / dysfunction protein, the other ones can compensate.

Annoyingly, 23andMe doesn't' actually tell us 'copy numbers'. which is kinda important for some genes like redheadedness. useful to know since many of the traits like that also impact dopamine and other important neurochemistry.

Fast Reading and Neurodiversity

Study Review

Summary of review

Reviewing the 12 studies listed in
Prevalence of Myocardial Fibrosis in Intensive Endurance Training Athletes: A Systematic Review and Meta-Analysis
for dietary information. This is in reference to a curiosity I raised in a tweet here

Per the article:

12 studies involving 1,359 participants were included for analysis. Among them, 163/772 participants in the endurance athletes group showed LGE positive, compared with 19/587 participants in the comparison group.

and they all appear listed in table 1.

"Table 1. Prevalence and patterns of myocardial fibrosis in athletic populations using CMR." ref

they are cited as 8-19 (which totals 12 as a sanity check)

The article also states they extract a bunch of data, but does not mention diet.

"Extracted items of the study included: author, year, country, design, sample size, number of athletes detected with MF, characteristic of endurance athletes and inactive controls, age, and gender."

I have broken them out with notes on details about diet below, as well as highlighting interesting findings.

Attempt to get official full text links were made. Sci-hub was used when applicable.

Tentative observations

My non-doctor and non-expert analysis: This seems so freaking rare and variable that grouping everyone together under a meta-analysis is freaking dumb as fuck. Are high-endurance athletes even dying of the complications of myocardial fibrosis anyway? And none of these studies look at diet factors and for the few that did find results, they all assume it's exercise damage without question, or consider it plausibly just normal feature of heart remodeling.

We do see a build up in what appears to be scar tissues (in a very small number) of endurance athletes tho. Why are a small number of athletes accruing such damage to their hearts at all, but not the majority of them. They all get big hearts... so something is failing to heal? That is odd.

Exploration of dietary data

cited as (8):

Myocardial late gadolinium enhancement: prevalence, pattern, and prognostic relevance in marathon runners


No data on diet.

Assumption is it's exersize associated.

Although the absolute number of marathon runners with LGE was low, the higher prevalence of LGE in runners than in control subjects suggests that the amount of exercise engaged in by the marathon runners may have had a role in the development of LGE.

cited as (9):

Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes


No data on diet.

Didn't run echocardiography on the control group.

Assumption is it's exersize associated.

Accurate diary recordings of the athlete's full training and competitive histories were collected. The data are unique in as much as all athletes were documented lifelong endurance athletes still competing in intensive endurance events.

The prevalence of LGE in veteran athletes was not associated with age, height, weight, or body surface area (P > 0.05), but was significantly associated with the number of years spent training (P < 0.001), number of competitive marathons (P < 0.001), and ultraendurance (>50 miles) marathons (P < 0.007) completed. An unexpectedly high prevalence of myocardial fibrosis (50%) was observed in healthy, asymptomatic, lifelong veteran male athletes, compared with zero cases in age-matched veteran controls and young athletes. These data suggest a link between lifelong endurance exercise and myocardial fibrosis that requires further investigation.

cited as (10):



No data on diet.

In contrast to previous reports, in this prospective study of a wide range of athletes with no known cardiovascular disease, clinically significant LGE was not observed in any sub-elite endurance athletes

cited as (11):

Right and Left Ventricular Function and Mass in Male Elite Master Athletes: A Controlled Contrast-Enhanced Cardiovascular Magnetic Resonance Study


No data on diet.

Based on our results, chronic right ventricular damage in elite endurance master athletes with lifelong high training volumes seems to be unlikely. Thus, the hypothesis of an exercise-induced arrhythmogenic right ventricular cardiomyopathy has to be questioned.

cited as (12):

No evidence of adverse cardiac remodeling in former elite endurance athletes


No data on diet.

Veteran endurance athletes who have performed regular strenuous endurance exercise over N30 years show a cardiac remodeling pattern characterized by larger LV, RV and LA cavities when compared with non-athletic healthy controls, with the greater LV size matched by an increased LV myocardial mass and with no evidence of permanent major cardiac damage or fibrosis assessed by imaging or blood biomarkers

cited as (13):

Lifelong Physical Activity Regardless of Dose Is Not Associated With Myocardial Fibrosis


No data on diet.

A lifelong history of consistent physical activity, regardless of “dose” ranging from sedentary to competitive marathon running, was not associated with the development of focal myocardial fibrosis.

cited as (14):

Prevalence of Subclinical Coronary Artery Disease in Masters Endurance Athletes With a Low Atherosclerotic Risk Profile


No data on diet.

This study seems to emphasize the difficulty of the processes of getting good LGE readings (refer "CMR Scan" heading). Mentioned that it was assumed LGE to be myocardio fibrosis.

LGE was considered to represent focal myocardial fibrosis.

No relationship was found between myocardial fibrosis and exercise intensity, years of training, or number of competitions.

cited as (15):

Exercise-induced arrhythmogenic right ventricular remodeling in master endurance athletes


No data on diet.

Whilst longitudinal surveillance is required to fully elucidate the clinical significance, the data suggest that chronic exercise may in some cases contribute to the development of an acquired arrhythmogenic cardiomyopathy

cited as (16):

Myocardial late gadolinium enhancement and T1 mapping in highly trained endurance athletes


No data on diet.

Highly trained endurance athletes showed higher prevalence of LGE than control subjects; always confined to the hinge point. Although this pattern of LGE may be another feature of the athlete’s heart, the results suggest that those with focal fibrosis might have globally higher myocardial ECV values

cited as (17):

Myocardial remodelling and tissue characterisation by cardiovascular magnetic resonance (CMR) in endurance athletes


No data on diet.

This one goes into some detail under "Focal myocardial fibrosis" on the controversy and plasuability of the findings. It suggests perhaps this is a normal phenomena and not related to a disease state?

It is speculated that the RV distention during exercise may result in chronic structural changes of the myocardial architecture, mainly in the septal points of insertion of the right ventricular wall. In our study, we found mild LGE in the inferior septal RV insertion in 23% of athletes. However, we did not consider this finding as true reactive MF. In fact, this finding was also observed in 36% of controls (figure 2). We believe that, as previously reported,17 19 plexiform fibrosis is a normal feature of the insertion-region anatomy that may result in contrast pooling within this area.

The conclusion states

In the only three athletes with focal MF, the LGE pattern observed suggests an intercurrent event not related with the remodelling phenomenon

cited as (18):

Myocardial Fibrosis in Competitive Triathletes Detected by Contrast-Enhanced CMR Correlates With Exercise-Induced Hypertension and Competition History


No data on diet.

This one seems to have more data about tri-athletes which includes distance factors. I wonder of longer distance training means a different diet.

LGE+ triathletes completed longer distances in swimming and cycling than LGE- triathletes, suggesting that race distances have an impact on the risk for myocardial fibrosis;

It has been suggested that increased wall stress and impaired resistance to physical stress in this region are potential explanations for involvement of the inferolateral wall in these diseases (28). This explanation may also apply to triathletes, who are characterized by repetitively increased wall stress under exercise.

The presence of scar tissue was associated with exercise-induced hypertension and increased left ventricular mass but also longer lifetime race distances. Therefore, the lifetime amount of exercise seems to affect the risk for myocardial scarring, at least in male triathletes.

The clinical relevance of myocardial fibrosis in competitive triathletes is currently unclear; however, myocardial fibrosis could be the substrate for cardiac arrhythmia with subsequent sudden cardiac death and a precursor for future heart failure. Therefore, future longitudinal studies are needed

cited as (19):

Cardiovascular magnetic resonance with parametric mapping in long-term ultra-marathon runners


No data on diet.

This one points out an interesting observation: high endurance athletes hearts would look like diseased hearts if you based it on reviews of diseased hearts in existing medical literature. The implication here is that if you only sample diseased hearts you will accrue bias.

The previously underestimated degree of adaptive volumetric structural changes of the heart in this group should raise caution when suspecting the presence of cardiomyopathy. Most of those athletes would fulfil the volumetric criteria for dilated cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy. Therefore those criteria, at least to the degree studied, should not lead to suspicion of cardiomyopathy in the absence of other changes not observed in healthy athletes such as globally decreased left or right ventricular function or the presence of regional wall motion abnormalities and/or symptoms and changes observed in other tests, as elegantly depicted in summative papers

They also have the assumption it is from exercise, the in this case they do at least have a correlation with one of the features they measure.

High intensity training may compromise the immunological system and predispose these individuals to myocarditis in cases of seasonal viral respiratory tract infections [31,32]. However, small, silent, mid-wall areas of fibrosis have also been found in almost 4% of general population [33]. If these presumably post-myocarditis residual changes are limited in size, such as in our study, they do not seem to carry increased risk of arrhythmias.

Review of endurance Athlete myocarditis…

Someone on twitter asked me

What does it really mean when people say that covid can alter your dna?

Like i get it in theory but i dont understand how it would work

and another person asked

Do you have any thoughts on horizontal gene transfer

Many viruses have a chance of inserting themselves in the DNA of a cell without actually triggering cell death or furthering replication. It is supposed to be rare in coronaviruses. Most of the ones that do this are known to be retroviruses

It seems to happen in some people with sars-cov-2 so when their cells die, the segments of viral dna are released. This is a suspected failure mode of PCR

The PCR failure thing is heavily pushed by conspiracy theory types to say that viruses don't exist. I don't hold that stance. Its fascinating because the DNA implantation does suggest that PCR itself may be flawed more than people believe

I think viruses can be friendly and helpful. There are viruses that live in mucus that specifically target and destroy pathogenic strains of bacteria. ("bacterialphages"). So the idea that viruses don't exist is absurd to me. But I can see why people would have doubts about PCR tests tho. Been thinking about this from before the pandemic hit.

There are all sorts of stories of weird faux pandemics thanks to faulty testing. So I'm inherently cautious here. There's a really illuminating story about Dartmouth Hitchcock's faulty whooping cough pandemic that is worth reading. I lived near this place for a while and some of my family have worked at it.

This has been termed "The false positive paradox"

Even a test with a very high 99% specificity (1% chance of false positives), when used to screen asymptomatic populations with a low background rate of actual infection, will yield high levels of false positives.

I am uncertain about PCR as a test myself. It does seem to have a much higher failure rate than is touted, and the amplification step they use does seem to be a bad way to actually measure infectious genetic material as a way to confirm someone is 'positive'. Some of the PCR techniques are better than others because they are designed to be used as diagnostics, but even then they wouldn't be able to distinguish genetic transfer from viral infection.

This is why I've been focusing on other signals besides just the PCR tests. With it being so hard to get testing done early on, we used head fevers as a proxy measure of infection. I also was hoping to see the data from waste-water plants. The CDC has only just recently started pushing this data out. The more signals we have, the easier it is to trust that the results from a test kit aren't a false positives.

I'd really like a reliable way to measure if someone is a carrier and able to transfer a virus without showing major symptoms. I don't think a single test is gong to work if the DNA can be modified like this, so it seems foolish to not also explore other ways of measuring. It has been an issue since the dawn of infectious disease research. Like the case of Typhoid Mary', who was a carrier of the disease that wasn't has heavily impacted. She apparently went on to spread it for a long time.

Some people believe this means there never was a virus and it is all human DNA, but I believe this is a mistake. That being said I do think the gene transfer effect happens more often than is commonly believed, but not so often it would explain it happening every time like purported by the conspiracy.

It's not even a new idea really. Horizontal Gene Transfer effects from viruses are also suspected as the cause of many virus derived cancer mutations. This has been a very rapidly improving area of research and is one of the reasons why I pay so much attention to DNA repair processes.

Been some research into it in the past, but not as much as I think there should be

How this impacts the person's gene expression? I am not sure. I do know if it happens to trigger any of the HERV-* pathways in the genes, it tends to be problematic.

I'm interested in HERV-* pathways because it is suspected of being a cause of triggering neurological disorders. In particular, strange ties to Multiple Sclerosis.

The research is still the first evidence of this retrovirus presence, in the severe COVID-19 patients' respiratory tract and plasma. The HERV-K presence — which also occurs in other diseases, such as cancer and multiple sclerosis — can be used as a biomarker associated with severity in COVID-19 cases. Its early detection could reinforce certain strategies use, such as anticoagulants and anti-inflammatory drugs

A lot of times these transpositions from virus to host are actually beneficial to the host' survival, so they get passed on thru evolution. I suspect many of these viral stretches of DNA are actually activated to induce hibernation. Its fascinating to think our bodies do this to learn patterns against disease.

My hunch is this is what 'long covid' is -> that HERV mechanism being triggered as a defense mechanism developed by an old virus in our genome.

But that is one of my unfounded crankpot ideas. I can't prove it, and its one of a number that might be possible.

I believe this is the term for the process that ends up triggering the host dna modification

I also suspect that this process is more normal than we realize and is perhaps a mechanism that drives horizontal gene transfer between bacteria etc.

I think part of the problem is we don't look for it because we don't have good mental models of how bacteria share genes and mate.

It these effects can cause changes in gut bacteria in fascinating ways.

Like how there was a carbohydrate digestion enzyme transferred from seaweed bacteria into the human gut bacteria in some people.

That mechanism has been investigated as a way to spread antibacterial resistance. So it's worth thinking about more critically than simply looking at it under the vaccine/virus lens.

CRISPR is one mechanism involved here, tho I am not sure how often viruses use it.

I don't know the rest of them. They are often used for intentional gene editing, particular ones that target "germ line" if they are meant to be passed on. We are still fairly 'green' at this process and I suspect there are more out there we don't know about.

Humans have mechanisms that fight this process in our own cells. But sometimes it doesn't work. People are trying to figure out how to stop this effect to enable gene therapy with it.

I personally think disabling CRISPR defense is very dangerous. There was a study that showed bacteria themselves use CRISPR as part of a combative process.

Some bacteria are resistant to it as well. It may be more widespread than believed.

Now, do Vaccines cause this? This idea keeps me up at night.

Horizontal Gene Transfer what?

I’m curious on your opinion about the notion that vaccines cause autism, do you think it has some accurate to it or no?

I don't believe the existing models of how vacccines cause autism are correct.

I'll leave you with this.

Its so much worse than anyone understands.

Moms infected during pregnancy who produce elevated levels of the cytokine IL-17a may have microbiome alterations that prime offspring for aberrant immune responses later in life, mouse study suggests
That one is from 1983

we've been using coronavirus to induce experimental autoimmune encephalitis.... the mouse model of neurodegenerative disease... for litterally 30+ years. It activates IL-17a and induces multiple sclerosis and other brain inflammation disorders.

Autism is an autoimmune disorder that is driven by gut microbiota and inflammation during development.

its the only answer that makes sense
vacccines are a red hering.

Even starvation of the mother can trigger it in offspring.

Vaccines trigger an infection response. But so do the viruses they are meant to protect from.

So I've been focusing on upstream -> feeding the immune system what it needs to avoid doing that.

Part of that is lipid function, part of that is gut bacteria, part of that is avoiding things that kill them, part of it is feeding them things to make them resiliant, and part of it is reducing my natural inclination toward inflammation driven by autoimmune genetics.

I plan to prove this one day.

Death is coming.

Death is coming.