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Gut Testing — Microbiome, Infection and Barrier Integrity

Most people arrive at a stool test having already decided what it will show. The useful version of the test does something less dramatic and more informative: it separates questions that look identical from the outside. Bloating with a raised calprotectin is a different clinical problem from bloating with a normal one. Loose stool with low pancreatic elastase is a different problem again. This panel exists to tell those apart, and to say plainly which of its markers can carry weight and which cannot.

Why the gut appears in a hormonal workup · What is measured · Which markers carry weight · When I use this panel · How I read these results · What to expect · Key takeaways · FAQ · References

Why the gut appears in a hormonal workup

Two reasons, and they are different from each other.

The first is inflammation. Mucosal inflammation is metabolically expensive and does not stay local; it competes for the same energy budget that ovulation, spermatogenesis and thyroid conversion draw on [Theoretical]. This page measures the gut end of that chain — barrier, immune signalling, energy competition — rather than explaining it.

The second is more specific and often overlooked. Oestrogens are conjugated in the liver and excreted into bile for elimination. Certain gut bacteria produce β-glucuronidase, an enzyme that cleaves the conjugate and returns free oestrogen to circulation.¹⁹ [Emerging — in vitro and human observational] Clearance is therefore not purely a hepatic matter: the composition of the gut community sets how much of what the liver has packaged for disposal actually leaves. When a cycle pattern and a steroid metabolite profile disagree with each other, this is one of the places the discrepancy can sit.

What is measured

A single stool sample, analysed by quantitative PCR. The panel is grouped below rather than listed exhaustively; the full report runs to several pages and we go through it together.

Enteric organisms — detection

Group	Reported
Bacterial pathogens	Campylobacter, Salmonella, Shigella/EIEC, Yersinia enterocolitica, Vibrio cholerae, C. difficile toxin A and B, pathogenic E. coli including Shiga toxin genes
Parasites	Giardia, Cryptosporidium, Entamoeba histolytica, Blastocystis hominis, Dientamoeba fragilis, Endolimax nana, helminths
Viruses	Norovirus GI/GII, adenovirus 40/41

Helicobacter pylori and virulence genes

Marker	What it shows
H. pylori	Presence of bacterial DNA in stool
cagA, vacA, babA, dupA, oipA, iceA	Which virulence determinants the strain carries — strains bearing cagA provoke a more intense mucosal inflammatory response than strains without it² [Established]

Commensal and opportunistic organisms

Relative abundance of the major commensal groups — Bacteroides, Bifidobacterium, Lactobacillus, Faecalibacterium prausnitzii, Akkermansia muciniphila, the Clostridia — reported alongside organisms that behave as opportunists when the community shifts, including Klebsiella, Pseudomonas, Citrobacter, Proteus, Morganella, Prevotella, Staphylococcus and Enterococcus. Fungi and yeasts, Candida species among them, are reported in the same way.

Digestive and inflammatory function

Marker	What it shows
Faecal calprotectin	Neutrophil migration into the bowel lumen — the marker that separates an inflammatory picture from a functional one³ [Established]
Pancreatic elastase-1	Exocrine pancreatic output; a low value explains fat malabsorption that dietary change alone does not correct⁴ [Established]
Steatocrit	Fat content of the sample, read alongside elastase
Secretory IgA	Mucosal antibody output at the epithelial surface [Emerging]
β-glucuronidase	Bacterial deconjugating activity — the enzyme described above
Anti-gliadin IgA	Mucosal antibody response to gliadin. This is not coeliac serology: tissue transglutaminase IgA with a total IgA is the diagnostic pathway, and a raised anti-gliadin here is a reason to arrange that, not a substitute for it⁵
Faecal occult blood	Reported. A positive result is a referral, not an interpretation
Eosinophil activation protein	Eosinophil involvement in the mucosa [Emerging]

Which markers carry weight

A panel this wide contains markers of very different quality, and a report that presents them in one uniform typeface invites you to read them as though they were equal. They are not.

The organism detection is the strongest part. Quantitative PCR for a named target is sensitive and specific, and it is the reason the panel is worth ordering at all. Two things are worth knowing about it. PCR detects DNA, not a living organism, so a positive result shortly after treatment can reflect residue rather than persistence. And for active H. pylori infection specifically, the urea breath test and the stool antigen test remain the validated diagnostics;⁶ a positive PCR here is a good reason to arrange one of those, and I do.

Calprotectin and elastase are the two markers that most often change what happens next. Calprotectin is used across the NHS to decide who needs endoscopy and who does not, which is exactly why it is useful here — it is the one number on this report that a gastroenterologist will recognise immediately and act on. Elastase answers a question that is otherwise very hard to answer without invasive testing.

β-glucuronidase and secretory IgA sit in the middle. The enzymology is well described and the direction of effect is not in doubt; what is less settled is how tightly a single faecal activity measurement tracks the recirculating load in an individual. I read a high value as a reason to look at the community that produces it, alongside a steroid metabolite profile — not as a number to be driven down.

The relative-abundance microbiome section is the weakest part of the report, and I say so. Stool sampling describes the luminal community leaving the body, which is not the same as the mucosal community; the reference ranges are population-derived rather than outcome-derived; and the same abundance pattern can accompany quite different clinical pictures. I read it as a pattern against a history, never as a set of values to be corrected toward a range. [Clinical Heuristic]

Zonulin: available as an add-on, and not ordered here

Zonulin is widely offered as the marker of intestinal barrier function. The evidence does not support that use, and the clearest demonstration comes from the group that discovered it. A 2018 study co-authored by Alessio Fasano found that the commercial ELISA does not detect pre-haptoglobin-2 — the protein zonulin was identified as — and instead recognises properdin and complement C3; subjects genetically incapable of producing the protein returned normal readings.⁷ A separate comparison of two commercial kits found them agreeing with each other at r = 0.29.⁸ The manufacturers have since relabelled the analyte “zonulin family peptides” without reformulating the assay, and no equivalent characterisation of the stool version has been published at all. [Established — negative] I therefore do not order it, and I do not read barrier integrity from a single number. Where the question is barrier function, the reasoning runs through calprotectin, secretory IgA, the organism picture, and the clinical history together.

When I use this panel

Where a gastrointestinal picture is part of the presenting problem rather than an aside: persistent bloating, altered stool form, reflux or upper abdominal pain, symptoms that began after travel or after a course of antibiotics, or a long-standing pattern that has been labelled functional without anything having been measured. In a fertility or endocrine workup specifically, I order it where a steroid metabolite profile and a cycle history do not agree, where inflammatory markers are raised without an obvious source, or where digestive symptoms have persisted alongside the hormonal picture for long enough that treating them separately has stopped making sense.

It is often ordered alongside Steroid Hormone Testing for the clearance question, or CardioMetabolic Testing where the inflammatory picture is the shared thread. The reasoning for reading them together is on Hormone Optimisation.

How I read these results, and what happens next

Results come back to a consultation. I read the report in the order of what it can support: organism findings first, then calprotectin and elastase, then the functional markers, then the abundance profile as context rather than as a target. What follows is a plan addressing the parts that are modifiable, with a repeat interval chosen to match the marker — calprotectin moves in weeks, a community profile does not.

This is testing that supports a personalised plan, not a diagnostic service. Where a result needs a doctor’s attention I say so plainly and write to your GP with the report.

What to expect

A single stool sample, collected at home in a kit posted to you, returned by prepaid courier. No fasting and no clinic visit are needed for the collection itself. Antibiotics, antifungals, bismuth-containing preparations and proton pump inhibitors all change what the sample shows, so note them in your intake form; there is usually a sensible interval to leave after finishing a course before you collect. Collection is postponed during an acute gastrointestinal illness and while there is visible blood in the stool, which needs assessing rather than sampling.

Fee: £400, inclusive of VAT. That covers the kit, the laboratory work, and the interpretation consultation — 45 minutes, in person in Wimbledon or online. Fees for every other panel are on the functional lab testing page.

Key takeaways

The panel separates presentations that look identical from the outside: bloating with mucosal inflammation is a different problem from bloating without it.
Quantitative PCR for named organisms is the strongest part of the report, and the main reason to order it.
Faecal calprotectin and pancreatic elastase-1 are the two markers most likely to change what happens next, and both are established in NHS practice.
Gut bacterial β-glucuronidase returns conjugated oestrogen to circulation, which makes clearance partly a gut question and not only a liver one.
The relative-abundance microbiome profile is the weakest section of the report; it is read as a pattern against a history, not as values to be corrected.
Zonulin is not ordered here. The commercial assay does not detect the protein it is named for — demonstrated by the group that discovered it.
One stool sample collected at home, with the interpretation consultation included in the fee.

Frequently Asked Questions

Is this the same as the NHS stool test my GP can arrange?

Partly, and the overlap is the useful part. Calprotectin, faecal occult blood and stool culture or PCR for enteric pathogens are all available through the NHS, and where your GP has already run them we use those results rather than repeating them. What this panel adds is the whole picture in one sample — the virulence genotyping, elastase, β-glucuronidase, the commensal profile — read together and against your history at a consultation rather than reported in isolation.

Will it tell me which foods to avoid?

No, and no stool test can. Food-specific antibody testing is not offered here: the antibodies mark exposure, frequently mark tolerance, and have no validated threshold or outcome trial behind them. Where food appears to be involved, a structured, time-limited and supervised reintroduction answers the question properly and costs nothing.

I have already had a microbiome test from a subscription service. Is this the same thing?

No. Those services sequence the community and return an abundance profile with a score. This panel includes an abundance profile, and — as above — it is the part I trust least. What it adds is the pathogen detection, the virulence genotyping and the functional markers, which is the part that carries clinical weight and the part those reports do not contain.

Can I have this without the initial consultation?

No. Testing is selected after an evaluation, because the value of a wide panel is in choosing the right one for a specific question. The same clinical context is what makes the interpretation of the results, and the recommendations that follow, reliable.

How often would it be repeated?

Only when there is a specific question to answer. Where an organism has been treated, a repeat at an interval agreed with whoever prescribed it makes sense. Where the change is dietary or the target is inflammation, three to four months is usually the shortest interval at which anything meaningful has moved. The abundance profile is not repeated routinely; it does not reward it.

References

Ervin SM, Li H, Lim L, et al. Gut microbial β-glucuronidases reactivate estrogens as components of the estrobolome that reactivate estrogens. J Biol Chem. 2019;294(49):18586–18599. doi:10.1074/jbc.RA119.010950 [Emerging — in vitro] ↩︎
Censini S, Lange C, Xiang Z, et al. cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc Natl Acad Sci U S A. 1996;93(25):14648–14653. doi:10.1073/pnas.93.25.14648 [Established] ↩︎
National Institute for Health and Care Excellence. Faecal calprotectin diagnostic tests for inflammatory diseases of the bowel. Diagnostics guidance DG11. 2013. [Established — guidance] ↩︎
Löser C, Möllgaard A, Fölsch UR. Faecal elastase 1: a novel, highly sensitive, and specific tubeless pancreatic function test. Gut. 1996;39(4):580–586. doi:10.1136/gut.39.4.580 [Established] ↩︎
National Institute for Health and Care Excellence. Coeliac disease: recognition, assessment and management. NICE guideline NG20. 2015. [Established — guidance] ↩︎
National Institute for Health and Care Excellence. Gastro-oesophageal reflux disease and dyspepsia in adults: investigation and management. Clinical guideline CG184. 2014, updated 2019. [Established — guidance] ↩︎
Scheffler L, Crane A, Heyne H, et al. Widely used commercial ELISA does not detect precursor of haptoglobin2, but recognizes properdin and complement C3. Front Endocrinol (Lausanne). 2018;9:22. doi:10.3389/fendo.2018.00022 [Established — negative] ↩︎
Ajamian M, Steer D, Rosella G, Gibson PR. Serum zonulin as a marker of intestinal mucosal barrier function: may not be what it seems. PLoS One. 2019;14(1):e0210728. doi:10.1371/journal.pone.0210728 [Established — negative] ↩︎
Flores R, Shi J, Fuhrman B, et al. Fecal microbial determinants of fecal and systemic estrogens and estrogen metabolites: a cross-sectional study. J Transl Med. 2012;10:253. doi:10.1186/1479-5876-10-253. PMID: 23259758. [Emerging — human observational] ↩︎

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