Stool testing Flashcards
Metabolic Endotoxaemia
‘An immune response that becomes a sub-clinical, persistent, low-grade inflammation because of increased circulating endotoxins (LPS)’.
Normally happens in conjunction with poor GI barrier integrity.
Can be a risk factor for many chronic diseases such as insulin resistance, diabetes, CFS, autoimmunity.
Comprehensive stool tests can evaluate:
- Microbial markers such as commensal bacteria, pathogenic bacteria, parasites, pathobiont microbes, mycology, sometimes worms (these are often best seen visibly in the stool).
- Host markers — markers made by the human host such as immune, digestive, inflammation, intestinal permeability and occult blood.
Methodologies of stool testing mostly include:
- Polymerase chain reaction (PCR) — DNA testing of the microbe, and doesn’t require a culture.
- Culture with MALDI-TOF or microbiology assessment.
Interpreting stool tests:
- When looking at stool testing, you are looking at a relationship between the individual person and their microbes. People may carry pathobiont microbes, without any issues to their health.
- We want to look for correlations of the symptoms + microbes + host markers.
- First and foremost, you must have taken a thorough case including GIT symptoms and dietary patterns to be able to interpret accurately.
- Use the interpretative guides provided by the lab doing the test, as each test will require a different reading. Note: Different stool tests will include different target markers.
- Reference ranges in the microbiome are hard to ascertain as there is a large range of normal, so don’t panic if something is in or out of range — look at the whole pattern.
- Different dietary models are well known for impacting the microbiota in different ways — so knowing the client’s diet is important to be able to read a stool test accurately.
Dietary model and Microbiota
Host markers — inflammation:
Calprotectin
Calprotectin: A protein made by leukocytes when they have migrated to and are active in the GI wall. It is a marker of inflammation
Flagged as high over 50 µg / g. Between 50‒175 is ‘mid-range inflammation’. The elevation is triggered by damage to the epithelial lining — in worst case scenarios IBD, ulcers, cancer, but in most scenarios, relates to pathogens, NSAIDS etc.
Lower inflammation, e.g.: ↓ gluten + sugar, ↑ vit. D3, fish oils (EPA+DHA), curcumin, polyphenols (e.g. quercetin), chamomile
Host markers — inflammation:
Eosinophil Protein X
- Normal range: <1.1 mcg / g; Moderate: 1.1–4.6 mcg / g; High: >4.6 mcg / g.
- Raised with intestinal inflammation and in cases of food allergies, parasites, colitis
Host markers — metabolic:
Beta-glucuronidase
An enzyme made by some intestinal bacteria.
- Elevated — often due to dysbiosis and a western diet ↑ in red meat / animal protein.
- When high it can interfere with oestrogen excretion (= ↑ circulating oestrogen)
Host markers — digestion:
Pancreatic elastase (PE-1)
Proteolytic enzymes excreted by the pancreas that do not breakdown in the GIT. Correlate with levels of amylase, trypsin etc.
- Normal range: 200–500 µg / g.
- < 200 µg / g — need digestive support.
- Exocrine (digestive) pancreatic insufficiency: 100–200 µg / g.
- Severe insufficiency: <100 µg / g.
A need for digestive support (e.g. minimising snacking, ↑ bitters dandelion greens, rocket, gentian etc.) — possibly low due to chronic stress, inadequate HCl, snacking
Host markers — digestion:
Faecal fats
Rough measure of fat in stool. Low accuracy as it changes with diet and testing type.
- ↑ levels suggest fat maldigestion associated with pancreatic insufficiency, SIBO, hypochlorhydria.
- ↓ levels — seen in low fat diets
Host markers ― immune:
sIgA (secretory IgA)
Secreted by mucosal tissue ― provides first line of immune defence in the GI mucosa.
- Low sIgA (<100 µg / g) ― correlates with chronicity. ↑ susceptibility to GI infections. Always identify why (e.g. chronic stress).
- High sIgA (<750 µg / g) ― upregulated immune response (e.g., acute GIT infection) when testing
Host markers ― immune:
Beta–defensin 2
Antimicrobial peptides produced by the GI wall when breached.
High >62ng / g ― might be a sign of the immune system responding to a breach by microbes, or due to GI inflammation e.g., UC.
Host markers ― intestinal permeability:
Zonulin family peptide
A peptide produced by epithelial cells when the GI tight junctions are open.
- High > 100 µg / g ― may be raised in severe intestinal permeability (e.g., due to poor nutrition, heavy metals, drugs, alcohol, dysbiosis) and coeliac disease.
- Note ― even if it is 0, it does not rule out other modes of ‘intestinal permeability.’ The patterns of microbes can also be clues to intestinal permeability.
Commensal bacteria
- One of the major indicators of health in the microbiota of humans is diversity.
- In the commensal markers, check for:
‒ Plenty of diversity (check that all bacteria are accounted for).
‒ Good levels of short-chain fatty acid producers (next slide).
‒ Good levels of Bifidobacterium (check that it is taking up more space than E. coli) and Lactobacilli. - Diets lacking diversity (e.g., junk food diet, FODMAP diet), over-eating, antibiotic usage and chronic conditions can impact these levels in an adverse way.
Short chain fatty acids (SCFAs)
- SCFAs are by-products of bacterial fermentation of fibre. The most common being butyrate, propionate and acetate.
- The epithelial cells of the colon use butyrate as their main fuel source — maintaining the intestinal lining.
- SCFAs can also affect appetite and modulate inflammation.
- Low SCFAs — caused by antibiotic use, low fibre diets, diarrhoea
