The Putrefactive Collapse Neurobiome Phenotype

GoodOnes Neurobiome · Phenotype · NEURO 06 Rebuild · ~2% of people

In plain terms

This is the deep-dysbiosis pattern — the rarest of the six and, by the measurement, the most disrupted. Butyrate capacity (both routes) has collapsed far below the cohort, bile-salt hydrolase reads low, and the putrefactive markers — p-cresol and polyamines — read high.

Butyrate is the main fuel for your gut barrier; when it collapses and putrefaction rises, the foundation of the gut-brain axis is affected at once.

Because so much moves together here, this is the most careful build — a barrier-repair formula and, given how deep the signal runs, a good moment to loop in your clinician.

The gut-brain mechanism, in depth

A healthy colon runs on saccharolytic fermentation — fiber to short-chain fatty acids, above all butyrate, which fuels the gut lining and keeps the barrier tight. In this phenotype butyrate capacity has collapsed and the community has shifted to putrefactive (proteolytic) metabolism: p-cresol (hpdB) and polyamines (speA/speC) read high, and bile-acid signaling reads low.

A leaky, under-fueled barrier plus a rising putrefactive load drives inflammatory tone and disrupts gut-brain signaling broadly — the pattern that tracks with inflammatory bowel disease in the data. The formula rebuilds the barrier and suppresses putrefactive producers by competitive exclusion, with NAD+ for cellular recovery; a butyrate potentiator is on the roadmap.

Your measured signature

Measured functional capacity across the 11 gut-brain pathways — read from targeted gene markers in your sequencing data (not inferred from which microbes are present), and CLR-normalized so pathways compare across people. In this phenotype (measured prevalence 2.1%, n = 86 of ~4,194 clustered samples) the standout readings are:

z = standard deviations from the cohort mean. These clusters come from the measured capacity alone and are not an artifact of sequencing batch (cluster/run agreement ≈ 0).

Signature chart — measured capacity across the 11 gut-brain pathways

How common is this phenotype?

Where your pattern sits among the six measured phenotypes:

Does this sound like you?

Framed as tendencies, not a diagnosis:

What the data shows

Across our microbiome dataset (n = 89 in this phenotype), these self-reported conditions were more common in this pattern than at baseline — associations, not a diagnosis:

Shown: associations passing FDR (q < 0.05).

FDR-significant (q<0.05) associations:

What your formula does

The matched formula’s action is BARRIER REPAIR + SUPPRESS putrefactive — repair the gut barrier while suppressing putrefactive producers by competitive exclusion.

Neuro-actives layered on the probiotic base:

Take it into your own hands

Your phenotype points to specific, self-directed levers — the “be your own biohacker” angle. None of this is medical treatment; it’s how to feed the pathway the measurement flagged:

• Increase diverse plant fiber as tolerated to rebuild butyrate producers — go gradually.
• Ease the putrefactive load by not overloading on excess protein relative to fiber.
• Add polyphenol-rich foods to favor beneficial producers.
• This is a clinical-tier pattern: work with your clinician alongside any formula.

One honest caveat

Your quiz result is a symptom-based pattern, not a verdict — and symptoms are orthogonal to biology, so a measured gut test is what confirms your true phenotype. Everything here is educational and non-therapeutic: formulas potentiate, suppress or support gut-brain pathways; they do not treat, cure or diagnose disease.

Your matched formula

Your result matches the GoodOnes formula built for this gut-brain pattern: Rebuild. Start there — or confirm your true phenotype first with a measured whole-genome (WGS) test.