Diagnostic Solutions Laboratory | GI-MAP & Food Sensitivity Tests

Cytokine Response Profile (CytoDx) – Diagnostic Solutions Laboratory The Cytokine Response Profile (CytoDx) by Diagnostic Solutions Laboratory provides a detailed look at how your immune system regulates inflammation and communication between immune cells. This advanced cytokine panel test measures key signaling molecules—called cytokines—that coordinate immune activity and influence how your body responds to infection, stress, and chronic illness. When cytokine levels become imbalanced, they can contribute to chronic inflammation, autoimmune reactions, or weakened immune defense. The CytoDx test helps identify these immune patterns, offering clinicians insight into your body’s inflammatory status and immune regulation at the cellular level. How the Test Works This test analyzes cytokines related to major immune pathways—Th1, Th2, Th17, and Treg cells. Each pathway plays a distinct role in immune defense, inflammation control, and recovery. Pro-Inflammatory Cytokines These markers promote immune activation and inflammation in response to infection or tissue damage: GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor): stimulates immune cell production IFN-γ (Interferon Gamma, Th1): activates macrophages and supports cellular immunity IL-1β, IL-2, IL-6, IL-7, IL-8, IL-12p70, IL-15, IL-17A (Th17), IL-18, TNF-α: key mediators of inflammatory and autoimmune processes MIP-1β (CCL4) and RANTES (CCL5): recruit immune cells to inflamed areas Elevated levels of these cytokines can indicate autoimmune disease, chronic infection, metabolic inflammation, or neuroimmune dysregulation. Anti-Inflammatory Cytokines These markers help calm the immune system and promote recovery: IL-4, IL-5, IL-13 (Th2): support antibody production and help reduce inflammation IL-10 (Treg): suppresses excessive immune activity to maintain proper regulation Low anti-inflammatory cytokine activity may contribute to unresolved inflammation, allergic reactivity, or autoimmune flare-ups. Clinical Meaning and Immune Patterns By mapping cytokine levels across immune pathways, the Cytokine Response Profile can reveal characteristic immune imbalances, including: Th1 dominance: associated with autoimmune or intracellular infection responses Th2 dominance: linked to allergies, asthma, and atopic conditions Th17 activation: connected to chronic inflammatory and autoimmune states Low Treg (IL-10): indicates reduced immune tolerance and regulation Identifying these immune signatures allows healthcare practitioners to create personalized treatment strategies that rebalance immune activity, reduce inflammation, and enhance long-term immune resilience. Who the CytoDx Test Is For The CytoDx panel is valuable for individuals with: Chronic fatigue, inflammation, or immune-related symptoms Autoimmune or allergic conditions Persistent or recurrent infections Signs of immune dysregulation or unexplained inflammation Summary The Cytokine Response Profile (CytoDx) from Diagnostic Solutions Laboratory offers a comprehensive assessment of immune signaling and cytokine balance. By pinpointing cytokine imbalances across Th1, Th2, Th17, and Treg pathways, clinicians can uncover hidden inflammatory drivers and design targeted interventions to restore immune balance, resilience, and optimal health.

If you have a GI-MAP report in front of you, here's what to know first: GI-MAP uses qPCR to detect microbial DNA — results are quantitative (CFU/g), not simple positive/negative Detection does not equal disease. Many markers are commonly present at low levels in healthy people Patterns across multiple markers matter more than any single result in isolation This guide explains every section of the Diagnostic Solutions GI-MAP report, including the complete opportunistic bacteria species list, individual marker interpretation, and the clinical patterns practitioners use to interpret results together WHERE DO I START? — JUMP TO YOUR RESULT A GI-MAP report can run 14+ pages. If you're looking at one specific flagged result, use this table to jump straight to the relevant section instead of reading top to bottom. If your report shows... Read this section H. pylori (positive or with virulence factors) H. Pylori and Virulence Factors Candida or other fungal markers Fungi / Yeast High Calprotectin Intestinal Health Markers — Inflammation Low Elastase-1 Intestinal Health Markers — Digestion High Streptococcus spp. Opportunistic Bacteria High Enterobacter spp. Opportunistic Bacteria High Zonulin Intestinal Health Markers — Add-On Markers High or Low SIgA Intestinal Health Markers — Immune Response Any named pathogen (Salmonella, C. diff, etc.) Pathogens Low Lactobacillus, Bifidobacterium, or Akkermansia Commensal / Keystone Bacteria Multiple abnormal markers across categories GI-MAP Result Patterns HOW TO PRIORITIZE A GI-MAP REPORT — THE WORKFLOW PRACTITIONERS USE Experienced practitioners don't read a GI-MAP report top to bottom. They work through it in a specific order, because some findings change the urgency of everything else on the page: Step 1 — Pathogens first. A positive pathogen result reframes the entire interpretation, since pathogens can directly explain symptoms that might otherwise be attributed to dysbiosis. Step 2 — H. pylori and virulence factors. Checked early because virulence-positive H. pylori changes treatment urgency independent of everything else on the report. Step 3 — Inflammation markers (Calprotectin, EDN/EPX). Establishes whether active gut inflammation is present — this contextualizes how seriously to weigh opportunistic bacteria findings later. Step 4 — Digestion markers (Elastase-1, Steatocrit). Poor digestion is a common root cause of downstream dysbiosis, so addressing it can sometimes resolve opportunistic overgrowth without targeting the bacteria directly. Step 5 — Dysbiosis (opportunistic bacteria, commensal bacteria). Now interpreted in the context of what's already been established — inflammation present or absent, digestion adequate or impaired. Step 6 — Immune markers (SIgA, Anti-gliadin IgA, Zonulin). Assessed last among individual markers, since they're often consequences of the issues identified in steps 1–5 rather than independent findings. Step 7 — Look for patterns across all categories. The final and most important step — see GI-MAP Result Patterns below for the specific multi-marker combinations practitioners look for. For a 60-second first pass, this same order works as a quick scan rather than a deep read: pathogens, then H. pylori, then Calprotectin (inflammation), then Elastase-1 (digestion), then SIgA, then Zonulin if tested, then opportunistic bacteria, then keystone bacteria last. The order doesn't change — only the depth of reading at each step does. WHAT IS THE GI-MAP TEST? GI-MAP (Gastrointestinal Microbial Assay Plus) from Diagnostic Solutions Laboratory is a stool test that uses quantitative PCR (qPCR) to detect microbial DNA in the gastrointestinal tract. Unlike older culture-based stool tests that only report positive or negative, qPCR measures the actual quantity of genetic material present, reported in colony-forming units per gram of stool (CFU/g). A result of 3.5e7 equals 3.5 × 10⁷ CFU/g — 35,000,000 CFU/g, or 35 million CFU per gram of stool. One CFU is roughly equivalent to one microorganism. GI-MAP is commonly ordered by functional and integrative practitioners for patients with IBS, chronic bloating, diarrhea or constipation, suspected dysbiosis, autoimmune conditions, chronic fatigue, skin issues, and food sensitivities. Reference ranges were developed using known positive, diseased samples to establish cutoffs that distinguish disease-causing levels of pathogenic and opportunistic microbes; pathogen reference ranges are correlated with an FDA-cleared assay for GI pathogens. The test can detect as low as 0.1 cell per gram of stool. Key interpretation principles: The test detects DNA, not live organisms — detection does not always mean active infection Quantity and clinical context matter more than simple presence/absence Some markers reflect colon activity specifically, not the small intestine Toxin genes may be detected even when toxins are not actively being produced — GI-MAP measures the genetic capability to produce a toxin, not toxin activity directly Mild elevations are common and are not always clinically treated Results must always be interpreted alongside symptoms and medical history, never in isolation HOW TO READ A GI-MAP REPORT Most GI-MAP reports are organized into these sections, in this order: Pathogens H. pylori and virulence factors Commensal / keystone bacteria Opportunistic bacteria Fungi / yeast Viruses Parasites Intestinal health markers (inflammation, immune response, digestion) Add-on tests (if ordered) Each result includes a quantitative level, a reference range, and visual flagging if elevated. A result shown as "1.21 × 10⁵" against a reference range of "0–1,000 CFU/g" (for example) represents 121,000 CFU/g — well above range, and would be flagged high. PATHOGENS The GI-MAP screens for bacterial, parasitic, and viral pathogens commonly associated with gastroenteritis. Not all individuals with a positive pathogen finding develop symptoms — the health of the individual, the transient nature of some pathogens, and the presence of virulence factors all affect whether symptoms appear. Common bacterial pathogens tested include Campylobacter, Clostridioides difficile (Toxin A and Toxin B genes), pathogenic E. coli strains (6 different gene types are measured separately from normal Escherichia spp.), Salmonella, Shigella/Enteroinvasive E. coli, and Yersinia enterocolitica. Clostridioides difficile — an important nuance: GI-MAP tests only for the genes for Toxin A and Toxin B, not the toxins themselves. Studies suggest 2–10% of the population carry C. diff, most asymptomatically. In asymptomatic patients with positive toxin genes, the genes are likely not "turned on" and not causing disease — though it remains prudent to avoid unnecessary antibiotics in these patients to prevent C. diff-associated diarrhea (CDAD). E. coli and Hemolytic Uremic Syndrome (HUS): Pathogenic E. coli strains carrying Shiga-like toxin genes are associated with a small risk of HUS, a serious kidney complication. Antibiotics may be contraindicated in suspected Shiga-toxin E. coli infections, as they can paradoxically trigger HUS by causing bacterial cell lysis and toxin release. Therapeutic framework for pathogens (the 5R Protocol): This is the standard clinical approach used by practitioners working with GI-MAP results, summarized here for reference: Step Focus Examples Remove Eliminate the pathogen/imbalance Antimicrobial herbs (berberine, caprylic acid, oregano oil, uva ursi), targeted antibiotics, antifungals, antiparasitics Replace Restore digestive capacity Betaine HCl, digestive enzymes, bile support, apple cider vinegar Reinoculate Rebuild beneficial flora Probiotics (Lactobacillus, Bifidobacterium strains), prebiotics (inulin, fiber, FOS) Repair Restore gut lining integrity L-glutamine, zinc carnosine, colostrum, immunoglobulins, S. boulardii Rebalance Address lifestyle factors Sleep, stress management, diet, exercise Practitioners typically re-test with GI-MAP 3–6 months after starting treatment to monitor progress. H. PYLORI AND VIRULENCE FACTORS GI-MAP detects H. pylori DNA along with a panel of virulence factor genes that indicate whether a detected strain carries markers associated with more aggressive disease. Virulence factor What it indicates CagA (Cytotoxin-associated gene A) The most studied virulence marker. CagA-positive strains are associated with significantly higher ulcer and gastric cancer risk; promotes DNA breakage in host cells VacA (Vacuolating cytotoxin A) Toxin that enters host cells by endocytosis and damages gastric epithelial cells; associated with ulcers and gastric cancer risk; antagonizes CagA BabA (Blood group antigen-binding adhesin) Helps H. pylori adhere to gastric mucosa; promotes DNA breakage especially alongside CagA; may promote carcinogenesis OipA (Outer inflammatory protein A) Promotes gastric inflammation; associated with carcinogenesis; often co-expressed with CagA DupA (Duodenal ulcer promoting gene) Promotes inflammation; associated with duodenal ulcers IceA (Induced by contact with epithelium) Transcription only initiated on contact with gastric epithelium; associated with dyspepsia and peptic ulcer disease in some populations VirB & VirD Part of the CagA "pathogenicity island" — both genes can potentiate CagA's virulence by aiding its transmission into host cells. Evaluate alongside CagA; if positive without CagA present, still clinically relevant in isolation A positive H. pylori result with one or more virulence factors — particularly CagA or VacA — generally warrants closer clinical evaluation than H. pylori detected without virulence markers. The absence of virulence factors does not eliminate clinical relevance; quantity and symptoms remain important. Elevated H. pylori is most clinically relevant when symptoms include reflux, stomach pain, ulcers, or nausea. COMMENSAL / KEYSTONE BACTERIA These are beneficial bacteria that play protective and regulatory roles in gut health. Key markers include Lactobacillus spp., Bifidobacterium spp., Faecalibacterium prausnitzii, Akkermansia muciniphila, Roseburia spp., and the Firmicutes and Bacteroidetes phyla. Low levels of keystone bacteria may indicate antibiotic exposure, poor diet, microbiome imbalance, or reduced gut resilience. Faecalibacterium prausnitzii and Roseburia spp. are particularly important as primary butyrate producers — low levels of these specific markers point toward reduced short-chain fatty acid production, which is associated with impaired gut barrier integrity and increased inflammation risk. OPPORTUNISTIC BACTERIA — COMPLETE SPECIES LIST Opportunistic bacteria are normally present in the gut but may contribute to symptoms when overgrown. Mild elevations are common and not always treated. High levels combined with elevated inflammation markers or low beneficial bacteria may suggest dysbiosis. Dysbiotic & overgrowth bacteria: Bacillus spp. Enterococcus faecalis Enterococcus faecium Morganella spp. Pseudomonas spp. Pseudomonas aeruginosa Staphylococcus spp. Staphylococcus aureus Streptococcus spp. Commensal & overgrowth microbes: Desulfovibrio spp. Methanobacteriaceae (family) Inflammatory & autoimmune-related bacteria: Citrobacter spp. Citrobacter freundii Klebsiella spp. Klebsiella pneumoniae Mycobacterium avium subsp. paratuberculosis Proteus spp. Proteus mirabilis Enterobacter spp. Escherichia spp. Fusobacterium spp. Prevotella spp. Individual marker notes for the most-searched species: Enterobacter spp. — Gram-negative genus in the Proteobacteria phylum, closely related to E. coli. High levels may indicate increased intestinal inflammatory activity. Low levels may indicate reduced mucosal health, since Enterobacter spp. is part of normal protective flora at baseline. Streptococcus spp. — Gram-positive bacteria that normally colonize skin and mucous membranes throughout the body. High levels in the intestine commonly result from low stomach acid, PPI use, reduced digestive capacity, SIBO, or constipation. Elevated levels may indicate intestinal inflammatory activity and can cause loose stools. Staphylococcus aureus — Gram-positive bacteria; high levels may result from reduced digestive capacity and intestinal inflammatory activity. Some strains produce toxins that contribute to loose stools or diarrhea. Morganella spp. — Gram-negative bacteria that may produce histamine. High levels may indicate increased intestinal inflammatory activity, can cause diarrhea, and are sometimes associated with SIBO. Citrobacter spp. / Citrobacter freundii — Gram-negative bacteria; high levels may indicate increased intestinal inflammatory activity. Citrobacter spp. has a documented association with rheumatoid arthritis (see autoimmune table below). Therapeutic approach for elevated opportunistic bacteria: High-dose probiotics (300+ billion CFU/day) Broad-spectrum antimicrobial herbs: berberine, caprylic acid, garlic oil, oregano oil, uva ursi, olive leaf extract Diet optimization: low sugar, low refined carbs, high plant-based foods and fiber Check SIgA to assess mucosal immunity and overgrowth protection Apply the 5R Protocol (above) If antibiotics are used, rifaximin is notable for remaining localized in the GI tract and is also used for SIBO Opportunistic bacteria and autoimmune associations: Organism Documented autoimmune association Citrobacter spp. Rheumatoid arthritis Fusobacterium spp. Systemic sclerosis, inflammatory bowel disease Klebsiella spp. Crohn's disease, ulcerative colitis, ankylosing spondylitis, and related spondyloarthropathies M. avium subsp. paratuberculosis Rheumatoid arthritis, Crohn's disease, Type I diabetes, possibly psoriasis Prevotella copri Rheumatoid arthritis Proteus spp. / Proteus mirabilis Rheumatoid arthritis and spondyloarthropathies Cytomegalovirus (CMV) Systemic lupus erythematosus, systemic sclerosis, type 1 diabetes, rheumatoid arthritis Epstein-Barr Virus (EBV) Rheumatoid arthritis, lupus, Sjögren's, multiple sclerosis, autoimmune thyroid disorders When gut barrier permeability is present (see Zonulin below), these microbes can potentially escape the gut lumen and contribute to triggering or sustaining autoimmune processes at extraintestinal sites — though GI symptoms are often less prominent when this mechanism is active, making the connection easy to miss without testing. FUNGI / YEAST Fungal organisms are commonly present in the digestive tract; overgrowth can cause illness in susceptible individuals. Fungal growth can be localized — Candida spp. may be elevated in the large intestine while normal in the small intestine, or vice versa. Fungi/yeast targeted on GI-MAP: Candida albicans, Candida spp. (commensal fungi that can become pathogenic in immunocompromised patients; may cause diarrhea and has been suggested, with weak evidence, to contribute to a cluster of symptoms including GI complaints, fatigue, and joint pain), Geotrichum spp. (may cause disease in immunosuppressed patients; low levels may simply be a dietary artifact from soft cheeses), Microsporidium spp. (specifically detects Encephalitozoon intestinalis; may cause diarrhea and wasting, can disseminate to ocular, genitourinary, and respiratory tracts), and Rhodotorula spp. Common causes of yeast overgrowth: antibiotic use, high intake of sugar/starches/dietary fungi (beer, bread, nuts, cheese, corn), hypochlorhydria, impaired immune function, and general dysbiosis. INTESTINAL HEALTH MARKERS Inflammation Calprotectin is the most studied marker of gastrointestinal inflammation and the gold standard for diagnosing and monitoring inflammatory bowel disease. High calprotectin indicates neutrophil infiltration to the gut mucosa. Immune Response Secretory IgA (SIgA) is the primary immunoglobulin in the intestinal mucosa, serving as a first-line defense against pathogens and antigens while also helping maintain microbiome balance. Low SIgA: suggests a suppressed gut immune system. Investigate chronic dysbiosis, antigen exposure, chronic stress, immunocompromise, or protein malnutrition. High SIgA: suggests an elevated immune response to antigens. Investigate chronic dysbiosis, acute infections, acute stress, or food sensitivities. Anti-gliadin SIgA indicates an immune response to gliadin (a gluten component) specifically within the gut — it does not necessarily correlate with blood antibody levels and does not diagnose celiac disease. Eosinophil Activation Protein (EDN/EPX) reflects eosinophil-driven gut inflammation with cytotoxic characteristics. Elevated levels are associated with respiratory allergies, asthma, food allergies, IBD, IBS, eosinophilic esophagitis, functional dyspepsia, acid reflux, intestinal barrier dysfunction, and intestinal parasites. In IBD specifically, EDN/EPX can be used to evaluate disease activity and predict relapse. Digestion Elastase-1 measures pancreatic enzyme output and is unaffected by pancreatic enzyme replacement therapy, making it a direct, uninfluenced indicator of pancreatic function. Fecal Elastase-1 result Clinical significance < 200 µg/g Pancreatic insufficiency 200–500 µg/g Decreased pancreatic output > 500 µg/g Normal pancreatic output Causes of low Elastase-1 include suppressed pancreatic function, gallstones, hypochlorhydria (particularly with concurrent H. pylori), cystic fibrosis, and low levels sometimes seen in vegetarians/vegans. Steatocrit measures fat in stool. High levels suggest maldigestion, malabsorption, or steatorrhea — caused by hypochlorhydria, pancreatic insufficiency, bile salt insufficiency, improper mastication, or celiac disease. Beta-Glucuronidase reflects microbial metabolism and enterohepatic recycling, particularly of estrogen via the glucuronidation detoxification pathway. Major bacterial producers include Bacteroides fragilis, Bacteroides vulgatus, Bacteroides uniformis, several Clostridium species, E. coli, and Staphylococcus. High levels may indicate colonic dysbiosis or SIBO, interference with Phase II detoxification (especially estrogen clearance), and in extremely elevated cases have been associated with increased colon cancer risk. Add-On Markers Zonulin is a protein that opens intercellular tight junctions in the gut lining, increasing intestinal permeability in the jejunum and ileum. It is considered a marker of "leaky gut" when elevated. Occult Blood (FIT) quantitatively measures hemoglobin in stool using antibodies specific to human hemoglobin, avoiding dietary restriction requirements and reducing false positives/negatives compared to older qualitative tests. Literature suggests a result of 10 µg/g may indicate potentially more serious conditions such as polyps or colorectal cancer, though common benign causes include hemorrhoids, anal fissures, pathogenic infection (e.g. Giardia), liver disease, and upper GI bleeding. GI-MAP RESULT PATTERNS — HOW PRACTITIONERS INTERPRET MULTIPLE MARKERS TOGETHER This is the single most clinically important section of the GI-MAP guide, and the part most poorly replaced by a quick AI summary: the lab's own clinical patterns combine multiple markers across categories into recognizable clinical pictures. Symptom → Likely GI-MAP Pattern Most people don't search by biomarker name — they search by symptom. This table maps common symptoms to the GI-MAP pattern most likely associated with them, each linking to the detailed pattern below. Symptom Likely pattern Bloating Methanogens (Methanobacteriaceae) + general dysbiosis Loose stool / diarrhea Pathogens, or high opportunistic bacteria Reflux / heartburn H. pylori Constipation Methanobacteriaceae (methane-dominant pattern) Histamine intolerance symptoms Morganella spp., Klebsiella spp./pneumoniae, and other histamine-producing bacteria Brain fog Dysbiosis combined with intestinal permeability (Zonulin) Food intolerance / new sensitivities Zonulin + SIgA + Anti-gliadin IgA pattern Fat malabsorption / greasy stool Low Elastase-1 + elevated Steatocrit Excessive gas (specifically) See Gas & Histamine Producers table below — hydrogen, methane, and hydrogen sulfide producers cause different symptom profiles Joint pain with GI symptoms Check Opportunistic Bacteria and Autoimmune Associations table — Citrobacter, Klebsiella, Proteus, M. avium This table is a starting point for which detailed pattern below to read first — it does not replace the full pattern tables, which include the complete marker list for each. Digestive Dysfunction Dysbiosis Pattern Dysbiosis associated with digestive dysfunction is very common and often stems from low stomach acid (hypochlorhydria), insufficient bile acids, poor digestion (pancreatic insufficiency or brush border enzyme deficiency), reduced absorption, and altered GI motility. Symptoms include excessive gas and bloating, abdominal discomfort, dyspepsia, heartburn, GERD, constipation or diarrhea, and food sensitivities. Marker category Typical direction Specific markers involved Pathogens Low to high Most types, especially if multiple pathogens present H. pylori Moderate to high With or without virulence factors Commensal/keystone bacteria High Enterococcus, Lactobacillus Phyla microbiota High Bacteroidetes and/or Firmicutes Opportunistic bacteria, yeast, protozoa Moderate to high Bacillus spp., Enterococcus faecalis/faecium, Morganella spp., Staphylococcus spp./aureus, Streptococcus spp., Methanobacteriaceae, Desulfovibrio spp., Klebsiella pneumoniae, Prevotella, Candida spp./albicans, parasitic protozoa Intestinal health markers Often low to moderately low Elastase-1 (low), Steatocrit (sometimes elevated) Food Intolerance, Allergy, and Adverse Food Reaction Pattern GI-MAP can be used alongside IgG/IgE food sensitivity testing to investigate the root cause of adverse food reactions. When the gut barrier is permeable and/or digestion is suboptimal, maldigested food proteins can trigger immune responses. Pattern category Markers Direction Histamine-producing bacteria Morganella spp., Pseudomonas spp./aeruginosa, Citrobacter freundii, Klebsiella spp./pneumoniae, Proteus spp./mirabilis, Enterobacter spp., Escherichia spp., Fusobacterium spp. High H. pylori H. pylori High Mast cell-activating bacteria Enterococcus faecalis, Pseudomonas aeruginosa, Staphylococcus aureus, Streptococcus spp. High Fungi/yeast Candida spp., Candida albicans High Lipopolysaccharide (LPS) producers (see LPS list below) High Commensal/keystone bacteria Lactobacillus spp. Low Intestinal health markers Eosinophil Activation Protein (EDN/EPX), SIgA, Anti-gliadin IgA, Zonulin High Gut Barrier Permeability ("Leaky Gut") Pattern Pattern category Markers Direction Intestinal permeability Any pathogen (high), Lactobacillus spp. (low), Akkermansia muciniphila (low/undetectable), Candida albicans (high), Anti-gliadin IgA (high), Zonulin (high) Mixed — see individual markers Low butyrate/SCFA production Faecalibacterium prausnitzii (low/undetectable), Roseburia spp. (low), Firmicutes phylum (low) Low Poor mucosal health Bifidobacterium spp. (low/undetectable), Escherichia spp. (low), Lactobacillus spp. (low), Akkermansia muciniphila (low/undetectable), Bacteroidetes phylum (low) Low Digestive Insufficiency Pattern Marker category Markers Direction Commensal/keystone bacteria Firmicutes phylum, Bacteroidetes phylum, Enterococcus spp., Lactobacillus spp., Akkermansia muciniphila High Opportunistic bacteria Bacillus spp., Enterococcus faecalis/faecium, Staphylococcus spp./aureus, Streptococcus spp., Desulfovibrio spp., Methanobacteriaceae, Fusobacterium spp. High Intestinal health markers Steatocrit (detected/high), Pancreatic Elastase-1 Steatocrit high, Elastase-1 low Gas & Histamine Producers Reference Table Category Organisms Primary hydrogen producers Faecalibacterium prausnitzii, Roseburia spp., Bacteroidetes phyla, Firmicutes phyla Primary methane producers Methanobacteriaceae (family) Primary hydrogen sulfide producers Bacteroides fragilis, Escherichia spp., Enterobacter spp., Desulfovibrio spp., Morganella spp., Pseudomonas aeruginosa, Staphylococcus aureus, Citrobacter spp./freundii, Klebsiella spp./pneumoniae, Proteus spp./mirabilis, Fusobacterium spp. Histamine-producing bacteria Lactobacillus spp., Morganella spp., Pseudomonas spp./aeruginosa, Citrobacter freundii, Klebsiella spp./pneumoniae, Proteus spp./mirabilis, Enterobacter spp., Escherichia spp., Fusobacterium spp. This table is particularly useful for patients with excessive gas, bloating, or suspected SIBO — matching symptom type (hydrogen-dominant vs. methane-dominant vs. hydrogen sulfide-dominant) to the specific bacterial drivers helps target treatment more precisely than treating "SIBO" as a single entity. Microbe Categories Associated with IBS & SIBO Category Organisms Mast cell-activating microbes H. pylori, Enterococcus faecalis, Pseudomonas aeruginosa, Staphylococcus aureus, Streptococcus spp., Candida spp./albicans, LPS producers Lipopolysaccharide (LPS) producing bacteria Escherichia spp., Enterobacter spp., Morganella spp., Pseudomonas spp./aeruginosa, Citrobacter spp./freundii, Klebsiella spp./pneumoniae, Proteus spp./mirabilis COMMON GI-MAP INTERPRETATION MISTAKES These errors lead to unnecessary treatment, missed root causes, and patient anxiety: Mistake 1 — Treating every elevated bacterium. Mild elevations of opportunistic bacteria are common in healthy people. Treating every flagged marker individually, rather than looking for a pattern that explains symptoms, leads to unnecessary and sometimes counterproductive antimicrobial use. Mistake 2 — Ignoring quantity. A result that is barely above the reference range is clinically very different from a result 100x above range, even though both are "flagged." Always check how far above (or below) range a result falls, not just whether it's flagged. Mistake 3 — Ignoring symptoms entirely. A lab report never overrides clinical presentation. A flagged marker in an asymptomatic person carries different weight than the same marker in someone with matching symptoms. Mistake 4 — Assuming PCR detection equals a live, active organism. GI-MAP detects DNA. DNA can be present from organisms that are not actively replicating or causing disease — this is explicitly why the lab itself states detection does not equal disease. Mistake 5 — Treating Candida just because it's detected. Candida is a normal commensal organism in many healthy guts. Mild detection without GI or systemic symptoms (bloating, sugar cravings, skin issues, brain fog) is not automatically actionable. Mistake 6 — Attempting to diagnose SIBO from GI-MAP alone. GI-MAP reflects colonic, not small intestinal, microbiota. SIBO requires breath testing. GI-MAP can suggest a SIBO-consistent symptom pattern (see gas/histamine producer table) but cannot diagnose it. Mistake 7 — Assuming low Lactobacillus alone indicates disease. A single low keystone bacteria marker, without other supporting findings (low SIgA, elevated opportunists, symptoms), is frequently a normal variation rather than a clinically significant finding on its own. Mistake 8 — Assuming H. pylori automatically requires treatment regardless of context. Many people carry H. pylori asymptomatically without virulence factors. Treatment decisions depend on virulence factor status, symptoms, and quantity — not detection alone. WHEN FINDINGS ARE PROBABLY NOT CLINICALLY SIGNIFICANT Not every flagged result needs action. These patterns commonly do not require treatment on their own: A tiny Candida elevation just above the reference range, without symptoms A single mildly elevated opportunistic bacterium, with no other abnormal markers and no symptoms Isolated Streptococcus spp. elevation with normal calprotectin and no GI symptoms Isolated SIgA elevation or reduction without accompanying inflammation or infection markers Isolated low Akkermansia muciniphila without other markers of permeability or low keystone bacteria A single H. pylori virulence factor detected without H. pylori itself being elevated In each of these cases, the result is worth noting and potentially monitoring at the next test, but does not typically justify aggressive treatment on its own. This is a useful filter before deciding what, if anything, to act on from a report with multiple flagged markers. WHICH GI-MAP MARKERS CHANGE FASTEST? This complements the repeat-testing guidance in the FAQ below — different markers shift on very different timescales, which affects when retesting will actually show meaningful change. Changes within days Changes within weeks Changes over months Pathogens (with treatment) SIgA Akkermansia muciniphila Calprotectin Candida Butyrate producers (Faecalibacterium, Roseburia) Occult blood Streptococcus spp. Overall microbial diversity Inflammation and infection markers respond fastest because they reflect acute immune activity. Opportunistic bacteria shift over weeks as antimicrobial or dietary interventions take effect. Keystone/beneficial bacteria and overall diversity are the slowest to rebuild — often requiring months of sustained dietary and probiotic support — which is why practitioners typically wait 3–6 months before a full retest rather than checking again after just a few weeks. FREQUENTLY CONFUSED MARKERS Several GI-MAP markers are commonly mixed up because they sound similar or appear in the same report section: Marker A Marker B Key difference Calprotectin Secretory IgA (SIgA) Calprotectin reflects neutrophil-driven inflammation (tissue damage signal); SIgA reflects mucosal immune defense activity (antibody response signal) — they can move independently SIgA Anti-gliadin IgA SIgA is the general gut immune defense marker; Anti-gliadin IgA is a specific subset measuring immune reactivity to gluten only Elastase-1 Steatocrit Elastase-1 measures pancreatic enzyme output directly (the cause); Steatocrit measures fat actually present in stool (the downstream effect) — low Elastase-1 often, but not always, produces high Steatocrit Zonulin Calprotectin Zonulin reflects gut barrier permeability ("leaky gut" — a structural issue); Calprotectin reflects active inflammation (an immune response) — permeability and inflammation often co-occur but are distinct mechanisms Opportunistic bacteria Pathogens Opportunistic bacteria are normally present and only problematic when overgrown; pathogens are not normal gut residents and their presence is inherently more concerning regardless of quantity GI-MAP VS OTHER STOOL TESTS Test Technology Strength Best for Biggest limitation GI-MAP qPCR Pathogen detection + virulence factor analysis + quantitative microbial DNA Pathogen and H. pylori virulence factor detail Does not diagnose SIBO; colon-focused, not small intestine GI Effects Culture + PCR + sequencing Broad gut function overview Digestion and absorption markers Less granular pathogen and virulence factor detail than GI-MAP GI 360 PCR + culture Balanced clinical stool panel General-purpose screening across categories Less detailed H. pylori virulence factor panel than GI-MAP Gut Zoomer Multiplex PCR + ELISA-based markers Broader autoimmune and zonulin/intestinal permeability focus alongside microbiome Autoimmune-pattern correlation, permeability markers Different clinical emphasis — less depth on quantitative pathogen load specifically GI-MAP is often chosen specifically when pathogen detection, H. pylori virulence factor analysis, and quantitative microbial DNA assessment are priorities — the virulence factor panel in particular (CagA, VacA, BabA, OipA, DupA, IceA, VirB, VirD) is a differentiator not commonly offered on competing stool panels. FREQUENTLY ASKED QUESTIONS Is GI-MAP accurate? GI-MAP uses qPCR technology, which is highly sensitive for detecting microbial DNA — down to as low as 0.1 cell per gram of stool. However, results must always be interpreted in clinical context: detection of DNA does not always indicate active infection or disease, particularly for organisms that are commonly present at low levels in healthy people. Does GI-MAP detect toxins? GI-MAP detects toxin genes, not toxin activity directly. A positive toxin gene result (for example, C. difficile Toxin A or Toxin B) indicates the organism carries the genetic capability to produce that toxin, but does not confirm the toxin is being actively produced or causing symptoms. Can GI-MAP diagnose SIBO? No. SIBO (small intestinal bacterial overgrowth) occurs in the small intestine and requires breath testing to diagnose. GI-MAP reflects microbes in the colon. However, GI-MAP can identify hydrogen, methane, and hydrogen sulfide-producing bacteria that correlate with SIBO symptom patterns (see the gas & histamine producers table above), which is useful supporting context even though it is not a SIBO diagnostic test itself. Can a GI-MAP test detect cancer? GI-MAP is not a cancer screening or diagnostic test. However, certain markers carry research associations with cancer risk that warrant mention: H. pylori with CagA and/or VacA virulence factors is associated with elevated gastric cancer risk in research literature, extremely elevated beta-glucuronidase has been associated with colon cancer risk in some studies, and a positive Occult Blood (FIT) result can be an early indicator warranting colonoscopy referral, since persistent GI bleeding is a recognized colorectal cancer symptom. None of these findings diagnose cancer — they identify risk factors or symptoms that may warrant further clinical evaluation, which is a meaningfully different thing. Are abnormal results always treated? Not always. Many findings reflect colonization or mild elevation rather than active disease. Treatment decisions depend on the magnitude of the finding, the patient's symptoms, and — critically — the overall pattern across markers, not any single result in isolation. What do H. pylori virulence factors mean? Virulence factors like CagA and VacA indicate that a detected H. pylori strain carries genes associated with more aggressive disease — higher ulcer risk and, in research studies, elevated gastric cancer risk. Their presence alongside a positive H. pylori result generally warrants closer clinical evaluation than H. pylori detected alone, without virulence markers. How often should GI-MAP be repeated? Many practitioners repeat GI-MAP after treatment or significant dietary changes — typically 3–6 months later — to confirm whether marker levels have shifted. Because the test is quantitative rather than simple positive/negative, retesting provides a direct, measurable before/after comparison rather than a binary result. What does it mean if Enterobacter spp. is high in stool? High Enterobacter spp. may indicate increased intestinal inflammatory activity. As a gram-negative organism closely related to E. coli, it is evaluated alongside other opportunistic markers and inflammation markers like calprotectin — an isolated mild elevation without symptoms or other abnormal markers is not necessarily clinically significant. What does it mean if Streptococcus spp. is high in stool? High Streptococcus spp. commonly results from low stomach acid, PPI (proton pump inhibitor) use, reduced digestive capacity, SIBO, or constipation. Elevated levels may indicate intestinal inflammatory activity and can contribute to loose stools. It is one of the markers in the "low stomach acid pattern" alongside elevated Enterococcus and H. pylori. WHAT DOES A MOSTLY NORMAL GI-MAP MEAN? This page focuses heavily on abnormal findings, but a substantial share of GI-MAP reports come back mostly or entirely within normal range. A normal report is genuinely useful information, not a non-result. Finding Interpretation No pathogens detected Reassuring — rules out the infections GI-MAP screens for Low/normal Calprotectin Good — no evidence of active gut inflammation Normal Elastase-1 (> 500 µg/g) Pancreatic digestive enzyme output is likely adequate Normal SIgA Mucosal immune defense appears balanced — neither suppressed nor overactivated Normal opportunistic bacteria levels No major dysbiosis detected in the markers tested Mild, isolated abnormalities with no symptoms Usually not clinically important on their own — see "When Findings Are Probably Not Clinically Significant" above Normal results reinforce each other. Just as practitioners look for clusters of abnormal findings pointing to the same pattern (see GI-MAP Result Patterns above), multiple normal findings together carry more weight than any single normal marker alone. Normal Calprotectin, normal SIgA, normal Elastase-1, normal Zonulin (if tested), no pathogens detected, and balanced keystone bacteria together make active inflammatory bowel disease, ongoing infection, and significant dysbiosis substantially less likely as explanations for symptoms — even though no single normal marker rules any of these out by itself. What a normal GI-MAP does not tell you: A normal GI-MAP does not exclude IBS, food intolerance, bile acid diarrhea, motility disorders, SIBO, or other functional gastrointestinal disorders. These conditions frequently occur with an entirely normal stool microbiome panel because they involve mechanisms — visceral hypersensitivity, motility dysfunction, bile acid malabsorption, small intestinal (rather than colonic) bacterial overgrowth — that GI-MAP is not designed to detect. A normal result narrows the differential; it does not close the investigation. HOW MUCH ABOVE RANGE ACTUALLY MATTERS? Not every elevated result carries the same clinical weight, and this is one of the most commonly missed nuances when reading a GI-MAP report. Elevation above reference range Typical significance Just above the upper limit Often a "monitor and recheck" finding rather than an immediate treatment trigger, especially if asymptomatic 2–5× the upper limit (ULN) More likely to be clinically meaningful, particularly alongside matching symptoms or other supporting markers > 10× the upper limit Usually warrants explanation and is less likely to be incidental This scale is a general guide, not a strict rule — three factors modify how much any given elevation matters: The organism itself. Some organisms (named pathogens, H. pylori with virulence factors) are concerning at any detectable level; others (mild opportunistic bacteria elevation) require much higher multiples above range before being clinically significant. Symptoms. A 3x elevation in someone with matching symptoms carries more weight than the same 3x elevation in someone asymptomatic. Patterns. A moderate elevation that's part of a recognized multi-marker pattern (see GI-MAP Result Patterns above) is more actionable than the same elevation in isolation. WHAT GI-MAP CANNOT TELL YOU Understanding a test's limitations is as important as understanding what it measures. GI-MAP cannot reliably determine: Whether detected organisms are alive and actively replicating — qPCR detects DNA, which can persist from non-viable or dormant organisms Whether dysbiosis is the cause of a patient's symptoms, as opposed to a coexisting but unrelated finding Antibiotic susceptibility of detected bacteria — GI-MAP identifies organisms and some resistance genes, but does not perform susceptibility testing the way a culture-based test can Exact anatomical location of an organism — GI-MAP reflects predominantly colonic content; it cannot distinguish small intestinal from colonic bacterial activity, which is why it cannot diagnose SIBO Disease severity — quantitative levels indicate how much DNA is present, not how severely a patient is affected clinically Treatment response after only a few days — most markers require weeks to months to shift meaningfully (see "Which GI-MAP Markers Change Fastest?" above); early retesting often shows little change even with effective treatment Future disease risk — with the narrow exception of specific documented associations noted earlier (H. pylori virulence factors and gastric cancer risk, for example), GI-MAP is not a predictive or risk-stratification test Being clear about what a test cannot do is as clinically useful as explaining what it can. A WORKED EXAMPLE — READING A SAMPLE REPORT Reading definitions in isolation is different from reading an actual report. Here is a fictional but realistic GI-MAP result set, interpreted the way a practitioner would actually work through it using the framework above. Sample results: H. pylori: negative Calprotectin: 22 µg/g (reference range typically < 50–173 µg/g depending on lab) Elastase-1: 580 µg/g SIgA: 1,900 µg/g (within typical 510–2,010 µg/g range) Candida spp.: normal Streptococcus spp.: slightly elevated, just above reference range Morganella spp.: normal Working through it using the priority order above: Step 1 — Pathogens and H. pylori: Negative. Nothing here reframes the interpretation. Step 2 — Inflammation (Calprotectin): 22 µg/g is well within normal range. No evidence of active gut inflammation. Step 3 — Digestion (Elastase-1): 580 µg/g is above the 500 µg/g threshold — normal pancreatic enzyme output (see staging table above). Step 4 — Immune markers (SIgA): 1,900 µg/g is within normal range, toward the upper end but not flagged — balanced mucosal immune activity. Step 5 — Dysbiosis (Streptococcus, Morganella, Candida): Streptococcus spp. is the only flagged marker, and only mildly so — just above range, not 2–5x or greater. Putting it together: This is a reassuring report. No pathogens, no inflammation, adequate digestion, balanced immune markers, and only one mildly elevated opportunistic organism with nothing else supporting a dysbiosis pattern. Applying the "how much above range matters" framework, a Streptococcus spp. result just above the upper limit, in the absence of elevated Calprotectin or other opportunistic bacteria, would typically fall into the "monitor" category rather than warrant aggressive antimicrobial treatment — particularly if the patient is asymptomatic or has only mild, nonspecific symptoms. If this patient has ongoing GI symptoms despite this reassuring panel, the "What a Normal GI-MAP Does Not Tell You" section above becomes directly relevant — IBS, bile acid diarrhea, SIBO, and motility disorders should be considered, since none of them would necessarily produce abnormal GI-MAP findings. GI-MAP INTERPRETATION CHECKLIST Before acting on any GI-MAP result — your own or a patient's — work through these questions: Is this organism actually above the reference range, or only flagged due to formatting? How far above (or below) range is it — barely flagged, or substantially elevated? Are the patient's symptoms consistent with what this marker typically causes? Is this finding supported by other markers, or is it isolated? Is this organism commonly found in healthy people at low levels? Does the quantity reported actually matter clinically, or is it within a range considered insignificant? Are multiple markers across categories pointing toward the same underlying pattern? Should this result be confirmed with a different test before treatment begins (e.g. breath testing for suspected SIBO, biopsy for suspected IBD)? Working through this checklist before treating any single result is the difference between targeted, effective intervention and reflexively treating numbers on a page. GI-MAP reports contain dozens of markers that change with diet, treatment, and time. HealthMatters lets you upload your GI-MAP report, view all markers clearly organized by section, track trends across multiple tests over time, and share results securely with your provider — turning a dense 15+ page lab PDF into something you can actually navigate and compare visit to visit. FINAL THOUGHTS GI-MAP provides a detailed view of gut microbes, digestion, inflammation, and immune activity. The most important interpretive principle — repeated throughout this guide and throughout the lab's own clinical documentation — is that results must be read in context and in combination, not reacted to one marker at a time. When used appropriately, GI-MAP helps identify patterns relevant to gut health and guides targeted clinical interventions. Understanding your report clearly, using the patterns and reference tables above, is the first step toward making sense of it.

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