This test is most useful if any of these apply to you.
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.
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.
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.
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.
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.
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.
| Tier | Range | What It Suggests |
|---|---|---|
| Normal | 0 to 60 | Microbial pattern is not strongly linked to active intestinal inflammation |
| High | Above 60 | Microbial 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.
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.
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.
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.
Evidence-backed interventions that affect your GI Effects Inflammation Score level
GI Effects Inflammation Score is best interpreted alongside these tests.