Irritable bowel syndrome (IBS) is increasingly understood not as a single-pathway disorder, but as a complex condition driven by interactions between the gut, brain, microbiome, and environment. In this interview, Lin Chang, a gastroenterologist at UCLA Health, explains how these systems shape symptom perception, dietary responses, and patient variability.
Why do some people with IBS react strongly to certain foods even when standard tests are normal?
In IBS, symptoms are not driven by structural abnormalities that show up on routine testing, but by altered gut-brain signaling, which can increase visceral sensitivity and alter gut function. Many patients have visceral hypersensitivity, meaning the gut is more sensitive to normal stimuli like gas, distension, or certain nutrients. Foods, particularly fermentable carbohydrates, can increase luminal distension through gas and fluid shifts, which may be perceived as pain or discomfort in a sensitized system.
In addition, gut microbiota composition, immune activation, and epithelial barrier function can influence how these food exposures are processed. So even when standard tests are normal, there are real physiologic differences in how the gut responds and how the brain interprets those signals.
How do you think about the role of the brain-gut axis in driving symptoms, especially in patients with normal clinical findings?
IBS is a disorder of gut-brain interaction, where symptoms arise from dysregulation across multiple levels of brain-gut interactions, involving peripheral or gut (motility, sensation, immune function), central nervous system (pain modulation), and autonomic nervous system, which can affect gut sensations, secretions, and motility. Even in the absence of overt inflammation or structural disease, there can be amplified signaling from the gut, altered central processing, and decreased descending pain inhibitory pathways, leading to heightened symptom perception.
Importantly, this is not "psychological" in a simplistic sense — it reflects integrated neurobiological processes, including stress responsiveness, autonomic imbalance, and central pain modulation.
What explains the level of variability in symptoms, both between different people and within the same person over time?
IBS is inherently heterogeneous, and symptoms can fluctuate over time. Between individuals, variability reflects differences in underlying mechanisms — for example, microbiome profiles, immune activation, motility patterns, central processing, comorbid conditions, and psychosocial factors. Within the same person, symptoms fluctuate due to interacting triggers such as diet, stress, sleep, and hormonal changes.
These factors influence the autonomic nervous system and brain-gut signaling, leading to day-to-day variability. This is why IBS is better understood as a systems-level disorder rather than a single-pathway disease.
Do dietary approaches like low FODMAP get at underlying mechanisms, or are they mostly helping with symptom control?
They do both, but primarily they are targeting downstream mechanisms. The low FODMAP diet reduces fermentable substrates, which decreases gas production and luminal distension — key triggers of symptoms in patients with visceral hypersensitivity. In that sense, it directly engages one of the mechanisms driving symptoms.
However, it is not currently thought to fundamentally correct upstream processes like central pain modulation or stress-related dysregulation. That's why we often think of dietary therapy as one component of a multidimensional, mechanism-based approach.
What areas of research or new treatments for IBS are you most excited about right now?
Several areas are particularly exciting. One is the use of digital and wearable technologies to capture real-world physiology — autonomic function, sleep, and circadian patterns — and link these to symptoms. Another is advancing our understanding of brain-gut-microbiome interactions through the integration of neuroimaging, microbial composition and metabolites, clinical symptoms, and systems biology approaches, which can help define subtypes within a heterogeneous disorder and guide personalized treatment.
I am also very interested in integrative digestive health treatment, which incorporates pharmacologic and non-pharmacologic approaches — for example, diet, brain-gut behavioral therapy such as cognitive behavioral therapy and gut-directed hypnotherapy, and acupuncture — from a multidisciplinary team (GIs, PCPs, GI dietitians, GI psychologists). Furthermore, it’s exciting that there are emerging non-pharmacologic neuromodulation strategies, including interventions that target autonomic function, such as vagal modulation.
From a clinical perspective, what do you think patients are missing when trying to understand or track their symptoms?
Many patients understandably focus on identifying a single trigger — often a specific food — but IBS symptoms typically arise from the interaction of multiple factors over time. What is often missed is the role of context, including chronic stress, sleep quality, hormonal cycles, risk factors (such as family history, psychological symptoms, early life adversity, and female sex), and prior exposures, which can modulate how the gut responds on any given day.
A better understanding of the complex brain-gut interactions — and how they can impact systemic function, homeostatic balance, clinical symptoms, and quality of life — is helpful to both patients and clinicians. In addition, symptom tracking is often too narrow or inconsistent to capture these patterns. Helping patients adopt a more integrated, biopsychosocial understanding and focus on patterns rather than isolated triggers can be much more effective for both understanding and managing symptoms.
Together, these insights reinforce a central idea: IBS is best understood as a dynamic, systems-level condition shaped by interacting biological and environmental factors. Moving beyond single-trigger thinking toward pattern recognition and personalized approaches may be key to improving symptom management and patient outcomes.