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Functional Gastrointestinal Disorders (FGIDs) majorpublished
Did you know?
A single gut–brain signal can travel from the intestine to the brain in under 100 milliseconds, fast enough to influence pain perception, motility, and even mood before you’re consciously aware of it. This speed is part of why functional gastrointestinal disorders feel so immediate and intense.
Functional Gastrointestinal Disorders (FGIDs)
Functional gastrointestinal disorders are symptom-based gut–brain interaction syndromes with no structural lesion, involving motility, visceral sensitivity, immune activation, dysbiosis, and central processing, diagnosed using Rome V criteria.
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Overview
Functional gastrointestinal disorders (FGIDs), now formally termed disorders of gut–brain interaction (DGBI), are chronic conditions defined by bothersome GI symptoms (pain, bloating, altered bowel habits, nausea, etc.) that occur without an explanatory structural lesion on routine testing. Rather than being “all in the head” or “nothing wrong,” they reflect measurable abnormalities in motility, visceral sensitivity, mucosal/immune function, gut microbiota, and central nervous system processing along the brain–gut–microbiome axis. FGIDs sit at the intersection of microbial dysbiosis, immune activation, and neuro-visceral modulation. Many patients show altered abundance of key fermenters (for example, SCFA-producing genera), shifts in gas-producing taxa, or instability in community structure, but no single microbial signature is universally diagnostic. Instead, pattern-based changes in function (e.g., SCFA output, bile acid metabolism, gas balance) are increasingly used to contextualize FGIDs within microbiome-signature frameworks and to guide microbiome-targeted interventions (diet, prebiotics, probiotics, postbiotics, fecal microbiota–based strategies).
Pathophysiology
FGIDs arise from a combination of:
Abnormal motility (e.g., delayed transit, spasm, impaired accommodation), Visceral hypersensitivity (lower pain thresholds to normal gut activity), Altered mucosal immune activation and barrier function, Changes in gut microbiota composition and metabolism, Central processing differences (stress responsiveness, pain modulation, cognitive–emotional factors). These processes are tightly coupled. For example, dysbiosis can promote low-grade mucosal inflammation and barrier leak, which amplifies sensory signaling and central pain processing. Conversely, psychological stress can alter motility, permeability, and microbial composition via autonomic and neuroendocrine pathways, completing a biopsychosocial loop characteristic of DGBI.
Classification (Rome IV)
Rome IV groups FGIDs/DGBI by anatomic region (esophageal, gastroduodenal, bowel, biliary, anorectal) and by age (adult vs pediatric). IBS, functional dyspepsia, and functional constipation are the most commonly encountered in practice. Diagnostic criteria are time-based and symptom-based, requiring symptom chronicity (≥3–6 months) and a minimum symptom frequency, with alarm features prompting evaluation for organic disease.
Summary Table
| Domain | Key concept for FGIDs/DGBI | Typical microbiome-related link |
|---|---|---|
| Definition | Symptom-based gut–brain interaction disorder (Rome IV) | No fixed lesion; functional dysbiosis patterns |
| Motility | Abnormal transit, accommodation, or coordination | Microbial metabolites modulate motility and secretion |
| Visceral sensitivity | Heightened pain to normal gut distension | Barrier leak and immune activation sensitize afferents |
| Mucosal/immune function | Low-grade inflammation, mast cell activation | Dysbiosis, altered microbial products, LPS exposure |
| Central processing/psychosocial | Stress, anxiety, trauma, coping styles | Brain–gut feedback alters composition and function |
| Clinical examples | IBS, functional dyspepsia, functional constipation, FAPDs | Subtype-specific microbial and metabolic patterns |
FGIDs thus represent network disorders of gut–brain–microbiome communication rather than “normal tests with unexplained symptoms,” making them highly relevant to any microbiome-driven clinical framework.
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Altered gut microbial profile is associated with abnormal metabolism activity of Autism Spectrum Disorder
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Short-chain Fatty Acids (SCFAs)
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