50 adults, 25 controls, 30 markers measured
Researchers publishing in Scientific Reports in 2025 measured 30 blood markers in 50 adults with atopic dermatitis, the most common form of eczema, and compared them with 25 people without the condition.
The trial found that several gut-derived markers ran higher in the eczema group. These included caproic acid, a protein called Reg3A, and two immune signalling molecules, interleukin-10 and interleukin-22.
One marker moved the other way. Trimethylamine, a compound gut bacteria produce from certain foods, was lower in the eczema group than in the controls.
None of this shows what caused what. It shows that the blood chemistry of adults with eczema looked measurably different from the blood chemistry of adults without it, on this set of 30 markers.
Why severity tracked with two fermentation byproducts
The more revealing pattern in the 2025 study was inside the eczema group itself, not between the eczema group and the controls.
The trial found that more severe eczema was associated with lower levels of caproic acid and isocaproic acid. Both are short-chain fatty acids made by gut bacteria as they ferment food.
This matters because short-chain fatty acids are known to interact with the immune system elsewhere in the body. A lower supply of them, in people with worse skin symptoms, is the kind of pattern that invites a mechanistic question rather than answers one.
The authors did not test why the association existed. They reported it as a correlation within their sample of adults with atopic dermatitis.
Fibre in, short-chain fatty acids out; protein in, indoxyl out
The Scientific Reports 2025 paper draws a specific chemical distinction that explains why fibre entered the discussion at all.
Short-chain fatty acids, including the caproic and isocaproic acid measured in this study, are produced when gut bacteria ferment fibre. Indoxyl, a different compound picked up in the same panel of markers, comes from bacterial breakdown of protein instead.
Because the marker that fell with rising severity was a fibre-fermentation product, the authors argue that fibre-rich diets deserve closer study in eczema. That is a research recommendation, not a demonstrated result.
No fibre intervention was tested in this paper. Nobody's diet was changed, tracked or compared. The claim is limited to the plausibility of a link, built on where these molecules come from.
One measurement, one moment, 75 people
The entire dataset behind these findings comes from 75 people, 50 with eczema and 25 without, measured at a single point in time.
That design can show association. It cannot show which came first, whether low caproic acid contributed to worse skin, whether worse skin changed gut bacteria, or whether some third factor drove both.
A cross-sectional study also can't rule out reverse causation or shared underlying causes, such as diet, medication use or disease duration, that weren't fully accounted for.
The researchers were explicit that this is association, not cause. Repeating the measurement in a larger group, or following the same people over time, would be needed before anyone could say more.
What this does and doesn't tell someone with eczema
This body of evidence says that adults with atopic dermatitis, in one 2025 sample of 50 people, showed a distinct blood chemistry signature, and that within that group, worse skin was associated with lower levels of two fibre-derived fatty acids.
It does not say that eating more fibre changes eczema outcomes. No trial in this dataset tested that question, and the paper itself calls for future research rather than reporting a result.
Anyone curious about their own gut bacteria or diet in relation to skin symptoms is dealing with an open scientific question, not a settled one. The honest position is that the biology is plausible and the sample size is small.
The next useful step, scientifically speaking, is a study that follows people over time or tests a dietary change directly, rather than a single blood draw compared across two groups.