The Environmental Basis of ME/CFSScott Daniska
An empty road running between pine woods under a heavy grey sky in a Florida state park.

I did not get better until I changed my environment.

A working model of ME/CFS, Long COVID and chemical sensitivity — built from nine years of testing it on myself.

My name is Scott Daniska. In 2017 I was a graduate student near the top of my PhD class. A chemical exposure in the lab I worked in ended that, and I have had ME/CFS ever since.

For four years I looked for the answer in the places everyone told me to look. I ran hundreds of tests. I read thousands of papers. I worked through every theory the patient community had on offer — B12 deficiency, craniocervical instability, microclots, mitochondrial disease, mast cell activation, genetics. Each one was either absent in my case or failed to respond to treatment. I filled two binders with results that came back normal.

What I had missed was sitting in the room with me. In 2021 I moved into an apartment that made me measurably worse, and for the first time the pattern was clean enough to see: I felt one way inside and another way outside. A mold test explained part of it. A mask fixed that part and did nothing for the rest, which turned out to be the varnish on the bedroom floor. When I moved again, a new building produced a new and entirely different set of symptoms.

That was the observation that reorganised everything. The symptom profile I had spent four years trying to explain as one disease was several exposures stacked on top of each other — some chronic, some acute, some transient. I had not been able to see it because there was never a single trigger to isolate.

What I think is happening

The model has two phases. In the first, something damages the epithelial barrier — a chemical exposure, a virus such as SARS-CoV-2, or an underlying connective tissue disorder. The barrier is what normally keeps airborne contaminants out of the body. Once it is compromised, ordinary indoor air becomes a source of continuous injury, and the damage outpaces repair.

In the second phase, insoluble nanoparticles enter through that opened barrier. I focus on titanium dioxide, because it is hard, abrasive, cleared from the body extremely slowly, and far more common than people realise — matte white paint is high in it, which means it is on the walls of most modern buildings. I do not think these particles are poisoning anyone. I think they are doing mechanical damage: tearing connective tissue, making blood vessels leaky, and clogging the interstitial spaces and lymphatics that the body relies on to clear waste and deliver oxygen.

If that is right, then a great deal of what looks like dysfunction in ME/CFS is better described as damage. That distinction matters. A dysfunctional system can be corrected with the right drug. A damaged one has to be protected long enough to repair, and cannot be while the exposure continues.

If you are a farmer and your plants are sick and dying, you do not conclude that they have a genetic, mitochondrial, psychosomatic disorder. You ask whether they are getting enough food, water and light. Why is it that with plants we accept that everything is environmental, and with people it never is?

Why I am publishing this

I have spent the last several years trying to get this in front of someone who could test it. I have contacted congressional offices, reporters, podcasts, medical conferences, ME/CFS advocacy organisations and individual researchers. Almost none of them replied. This site exists because the work should be readable by anyone who wants to evaluate it, without needing me to be granted a platform first.

I am not selling anything and I do not have a treatment protocol. What I have is a mechanism, a body of personal evidence, and a set of predictions that could be tested by people with better equipment than mine.

The Model

The mechanism in six stages, from barrier injury to systemic failure.

Evidence

Imaging, biopsy, capillaroscopy and clinical photographs, with what each one shows.

My Story

2017 to now, including the four days that changed the course of the illness.

What this site is. This is independent research by a patient with a science background, not peer-reviewed work and not medical advice. The mechanism described here is a hypothesis. I have tried throughout to separate what I observed from what I infer, and to mark clearly where I am uncertain.