Instalab

GI Effects Inflammation Score Test Stool

Get an early read on whether your gut bacteria and inflammation are pulling in the same direction.

Should you take a GI Effects Inflammation Score test?

This test is most useful if any of these apply to you.

Living With Ongoing Gut Symptoms
If you have persistent bloating, pain, or irregular stools and standard tests look unremarkable, this can show whether bacterial imbalance and inflammation overlap.
Family History of IBD or Autoimmunity
If a close relative has Crohn's, ulcerative colitis, or autoimmune disease, tracking this gives you a baseline before symptoms develop.
Recovering From a Long Antibiotic Course
If you have just finished extended antibiotics, this offers a structured way to see whether your gut community is rebalancing or staying disrupted.
Healthy but Want to Stay Ahead
If you are proactively managing your health, this gives an exploratory window into whether your gut environment is drifting before symptoms appear.

About GI Effects Inflammation Score

When your gut feels off, the question is rarely just whether you have inflammation or just whether your bacteria look unusual. It is whether the two are tangled together, with each one feeding the other. The Inflammation-Associated Dysbiosis score tries to answer exactly that question by combining what your gut bacteria look like with markers of inflammation in the same stool sample.

This is an exploratory measurement rather than an established clinical test. It does not diagnose disease on its own, and the cutpoints come from one company's database rather than from broad medical consensus. Used as a trend marker alongside other gut and inflammatory tests, it can give you a structured way to track how your gut environment is changing over time.

What the Score Actually Measures

The IAD (Inflammation-Associated Dysbiosis) score is a proprietary algorithm built into the GI Effects stool panel. It blends gut bacterial composition with fecal beta-glucuronidase (an enzyme produced by certain gut bacteria) and fecal calprotectin (a protein released by your immune system's first responders, called neutrophils, when they enter the gut wall). Higher scores correlate with higher calprotectin, higher eosinophil protein X (a marker of allergy-type immune cells), higher secretory IgA (an antibody your gut makes), and lower amounts of normal commensal bacteria, which are the everyday bacteria that keep your gut working properly.

The score is reported in arbitrary units on a 0 to 100-style scale, with a manufacturer-defined cutoff of 60. A result above 60 is considered high and points toward intestinal inflammation linked to microbial imbalance. A result at or below 60 is considered within the normal range. Because the score is calculated from a specific bacterial database and lab method, it is not interchangeable with other dysbiosis indices on the market.

Why a Combined Score Can Reveal More Than Single Markers

Standard inflammation markers like fecal calprotectin tell you whether immune cells are active in your gut, but not why. A microbiome report alone tells you which bacteria are present, but not whether your immune system is reacting to them. The IAD score is designed to flag the overlap, where the bacterial pattern lines up with active inflammation.

Across studies of people with inflammatory bowel disease, dysbiosis indices show good ability to separate disease from controls. A pediatric microbiome classifier for inflammatory bowel disease (IBD) reached an AUC of about 0.83 to 0.84, meaning it correctly distinguished cases from controls about 8 to 9 times out of 10. Adult IBD models using broader bacterial sequencing reached AUCs above 0.90. The IAD score itself is described as validated in an IBD cohort, though specific sensitivity and specificity numbers have not been published.

Inflammatory Bowel Disease

Patients with Crohn's disease and ulcerative colitis show significantly higher IAD scores and higher inflammatory markers than healthy controls. Higher scores in this group track with the underlying problem these conditions cause: a chronic mismatch between gut bacteria and the immune system, with loss of beneficial bacteria that produce short-chain fatty acids (the main fuel for cells lining your colon) and a rise in groups like Enterobacteriaceae that can trigger inflammation.

The score is not specific to one diagnosis. People with celiac disease or irritable bowel syndrome (IBS) have shown IAD and inflammatory marker patterns similar to healthy controls in the validation work, even when they have ongoing GI symptoms. So a normal IAD does not rule out a functional gut disorder, and an elevated IAD does not by itself confirm IBD.

Other Conditions Linked to Dysbiosis Patterns

Beyond IBD, microbiome and inflammation patterns related to dysbiosis show up in several other settings. In a small study of nine women with endometriosis, three had IAD scores above 60 alongside elevated beta-glucuronidase and secretory IgA, suggesting dysbiosis-linked inflammation in a condition usually thought of as gynecologic. In acute decompensated cirrhosis, the gut barrier becomes highly inflamed and permeable, with elevated stool cytokines and calprotectin. In systemic sclerosis, intestinal dysbiosis and elevated fecal calprotectin associate with esophageal motility problems, malnutrition, and lung fibrosis.

In older adults, elevated fecal calprotectin (one of the inputs to the IAD score) tracks with gut microbial dysbiosis and a higher prevalence of obesity and prior heart attack. The point is not that this score predicts heart disease, but that the underlying biology it tracks is part of the broader story connecting gut health, inflammation, and chronic disease.

Reference Ranges

These cutpoints come from the manufacturer's IBD validation database, not from broad population studies, and have not been adopted by major medical guidelines. Treat them as orientation rather than as universal targets, and compare your results to your own previous values from the same lab.

TierRangeWhat It Suggests
Normal0 to 60Microbial pattern is not strongly linked to active intestinal inflammation
HighAbove 60Microbial pattern is consistent with inflammation-associated dysbiosis; pairs with elevated inflammatory and immune markers in validation cohorts

Source: Genova Diagnostics IAD validation work using IBD and celiac cohorts. The score is calculated from a specific stool assay and bacterial reference database, so values are not interchangeable with other commercial dysbiosis indices.

Reconciling Confusing Patterns

Two patterns can confuse readers. A normal IAD with elevated inflammatory markers means your bacterial pattern is not the obvious driver, and other causes of inflammation should be investigated. A high IAD with normal inflammatory markers is harder to interpret, and the published guidance is that the meaning of this combination still requires longitudinal research. Both situations are reminders that this is a pattern marker, not a yes-or-no disease test, and that it works best alongside other measurements.

Why One Reading Is Not Enough

Gut bacteria fluctuate substantially even in healthy people. In one study of healthy women sampled daily for six weeks, most bacterial groups changed dramatically from day to day, sometimes by 100-fold, and within-person variability often exceeded between-person differences. Stool moisture and recent diet were the strongest drivers. In hospitalized patients with acute myeloid leukemia, antibiotics were the only clinical factor that consistently increased microbiome instability over time.

Because of this variability, a single reading of any microbiome-derived score, including IAD, can be misleading. A practical approach is to get a baseline, retest in 3 to 6 months if you are making targeted changes (diet, treating an infection, addressing a known dysbiosis), and at least once a year after that to track your trend. Look for direction and persistence, not single numbers.

When Results Can Be Misleading

  • Recent or current antibiotic use: broad antibiotic exposure substantially shifts gut bacteria for weeks to months and can transiently produce a dysbiosis-like pattern that does not reflect your steady state.
  • Proton pump inhibitors (PPIs): these acid-blocking medications lower microbial diversity and shift composition toward an oral and potentially pathogenic profile, even though they are treating acid problems rather than gut inflammation. Population work has shown PPI effects on the microbiome can be larger than the effects of antibiotics.
  • NSAIDs and opioids: these drugs can cause gut inflammation, increased permeability, and microbiome shifts that mimic disease patterns without an underlying chronic gut disease.
  • Strenuous exercise in the prior 24 to 48 hours: prolonged intense activity, especially in heat, can transiently increase intestinal permeability and inflammation, then normalize. Sampling soon after a hard workout can produce a misleading high reading.

What to Do With an Elevated Result

An above-60 score on its own should be treated as a signal to investigate, not a diagnosis. The most useful next steps are pairing the result with fecal calprotectin (active intestinal inflammation), secretory IgA (mucosal immune activation), eosinophil protein X (allergy-type immune cells in the gut), and a markers-based or PCR test for gut pathogens. If you have ongoing GI symptoms, blood in stool, unexplained weight loss, or a family history of IBD, an elevated IAD is reason to bring the result to a gastroenterologist for evaluation that may include colonoscopy. If you are otherwise well, retesting after addressing obvious confounders (recent antibiotics, PPIs, NSAID use) is the cleaner first move before committing to interventions.

What Moves This Biomarker

Evidence-backed interventions that affect your GI Effects Inflammation Score level

Increase
Proton pump inhibitor (PPI) therapy
Long-term PPI use lowers gut microbial diversity, enriches oral and potentially pathogenic bacteria, and shifts the gut community toward a less healthy profile. In population-level studies, PPI effects on the microbiome were more prominent than those of antibiotics or other commonly used drugs. This shift affects the bacterial inputs to the IAD score and can also raise the risk of enteric infections like C. difficile, so the upward pressure on the score reflects real biological harm to the gut community.
MedicationStrong Evidence
Increase
Broad-spectrum antibiotic courses
Broad antibiotic exposure substantially reduces gut bacterial diversity and increases microbial instability for weeks to months. In hospitalized patients, total days on antibiotics was the only clinical factor consistently linked to greater microbiome instability and higher infection risk. Because the IAD score depends on bacterial composition, antibiotic courses can push it upward and make any single result unreliable for that period.
MedicationStrong Evidence
Decrease
Mesalamine dose escalation in ulcerative colitis
If you have quiescent ulcerative colitis, increasing your mesalamine dose can lower fecal calprotectin, one of the inflammation inputs to this score, and reduce relapse risk. In a randomized trial of 119 patients, an extra 2.4 g per day of mesalamine reduced fecal calprotectin levels and was associated with fewer relapses. The effect on the full IAD score has not been directly measured, but lowering calprotectin tends to pull the composite score downward.
MedicationModerate Evidence
Decrease
Mediterranean diet pattern
Following a Mediterranean eating pattern (heavy in vegetables, legumes, olive oil, fish, and whole grains) reduces intestinal inflammation and reshapes the gut bacterial community in a more anti-inflammatory direction. In a randomized trial of 28 adults with quiescent ulcerative colitis, a Mediterranean pattern reduced inflammation markers and shifted the bacterial profile favorably. A separate randomized trial in 82 overweight and obese adults found bacterial and metabolic improvements independent of calorie change. Both inflammation and bacterial inputs to the IAD score move in the desirable direction with this pattern.
DietModerate Evidence
Decrease
Multi-strain probiotics
Probiotics can strengthen the gut barrier, reduce circulating endotoxin, and lower inflammatory markers. A meta-analysis of randomized trials found probiotics improved intestinal barrier function and reduced inflammation and microbial dysbiosis. In a randomized trial of 74 people with Parkinson's disease, a four-strain probiotic enriched gut bacteria and reduced inflammation. Effects on the specific IAD composite score have not been directly tested, but the inputs (inflammation markers and bacterial composition) shift in directions consistent with a lower score.
SupplementModerate Evidence
Increase
Diet high in ultra-processed foods
Diets dominated by ultra-processed foods are linked to lower microbial diversity, reduced barrier integrity, and immune activation, and to higher risk of inflammatory bowel disease. A systematic review of human evidence found high ultra-processed food intake associated with intestinal dysbiosis that may promote immune-mediated diseases. Both bacterial and inflammatory inputs to the IAD score move in unfavorable directions on this pattern.
DietModerate Evidence
Decrease
Regular moderate-intensity exercise
Sustained moderate exercise increases gut bacterial diversity, supports short-chain fatty acid production, and reduces intestinal inflammation. Systematic reviews of physical activity studies show moderate exercise enhances motility, reduces inflammation, and supports microbial balance, while very high-intensity training can transiently worsen leaky gut and inflammation. The net effect of regular moderate activity on the IAD inputs is favorable.
ExerciseModest Evidence

Frequently Asked Questions

References

25 studies
  1. Quaglio a, Grillo TG, De Oliveira EC, Di Stasi LD, Sassaki LWorld Journal of Gastroenterology2022
  2. Di Vincenzo F, Del Gaudio a, Petito V, Lopetuso L, Scaldaferri FInternal and Emergency Medicine2023
  3. Heinzel S, Jureczek J, Kainulainen V, Nieminen AI, Suenkel U, Von Thaler AK, Kaleta C, Eschweiler GW, Brockmann K, Aho V, Auvinen P, Maetzler W, Berg D, Scheperjans FScientific Reports2024
  4. Riva a, Gray EH, Azarian S, Zamalloa a, Mcphail M, Vincent R, Williams R, Chokshi S, Patel V, Edwards LJHEP Reports2020
  5. Andreasson K, Alrawi Z, Persson a, Jonsson G, Marsal JArthritis Research & Therapy2016