LaBGAS studies the two-way traffic between the gut and the brain in humans. Our common thread is that bodily signals — mechanical, chemical, nutritional, immune and microbial — do not simply report on the state of the body; they shape perception, appetite and affect, and they do so through mechanisms we can measure and manipulate experimentally.

Three research lines organise that work. They overlap heavily in method and in people.

Gastrointestinal symptom, pain, and fatigue perception

This line asks why some people experience severe, disabling gastrointestinal symptoms with little detectable organic abnormality while others with clear pathology report almost nothing. We study symptom perception in disorders of gut-brain interaction — irritable bowel syndrome, functional dyspepsia, refractory reflux — and in related functional somatic syndromes, combining controlled gut stimulation with brain imaging, psychophysiology and experimental manipulations such as fear conditioning, returning to visceral hypersensitivity, interoceptive fear learning and hypervigilance.

Fatigue has become a substantial strand of this line. It has traditionally been studied either as (psycho)physiological dysfunction — of the stress response, immune and central nervous systems — or, in health psychology, as distorted perception of bodily sensations; we integrate the two, since neither alone explains why fatigue is experienced as severely as it is. We pursue this through the gut-immune-brain axis in both myalgic encephalomyelitis/chronic fatigue syndrome and inflammatory bowel disease, where half of patients in remission remain fatigued despite anti-inflammatory treatment.

Related work examines the bidirectional sleep-pain relationship in chronic low back pain.

Appetite, food intake & reward

This line investigates how gastrointestinal signals act on the homeostatic and hedonic brain circuits that regulate appetite, feeding behaviour and ultimately body weight.

We deliver nutrients and tastants directly to the stomach or duodenum — often below the threshold of conscious perception — and measure the consequences for gut hormone release, brain responses, subjective appetite, emotion and food intake. Neurotransmitter systems including dopamine, opioids and endocannabinoids are studied with PET and simultaneous PET-MR imaging.

Applied questions include whether non-caloric sweeteners such as erythritol can reproduce the satiating and rewarding properties of sugar, what changes in food reward after bariatric surgery, and how to select patients for GLP-1-based pharmacotherapy across the binge-eating spectrum.

Microbiota, gut signals & the mind

Our most recent line asks how nutrient- and microbiota-derived signals from the gut influence psychological processes and their neural basis — particularly the response to psychosocial stress, fear learning and extinction, executive function, and affect.

The flagship project is MoodBugs, funded by an ERC Consolidator Grant, which tests short-chain fatty acids and inflammation as mediators of human microbiota-affect relationships. Related work examines butyrate as an epigenetic modulator of fear memory, probiotic effects on academic stress, and the role of microbial metabolites in anorexia nervosa.

Projects

Symptom perception projects

DISCOvERIE

Comorbidities of IBS across Europe Development, diagnosis and prevention of gender-related somatic and mental comorbidities in irritable bowel syndrome, and the central nervous system mechanisms that underlie them. EU Framework Programme for Research and Innovation (Horizon 2020) · 2020-2024

Irritable bowel syndrome (IBS) is a common chronic functional gastrointestinal (GI) disorder characterized by abdominal pain and altered bowel habits. Etiologically, IBS is defined as a disorder of gut-brain interaction, but the exact underlying pathophysiological mechanisms of IBS are incompletely understood. Different mechanisms have been demonstrated on several levels of the gut-brain axis, including host genetics, microbiota composition and function, mucosal barrier function, mucosal and systemic immunity, low-grade inflammation, GI motility, neuroendocrine stress sensitivity, the function of nociceptive and cognitive-affective neurocircuits, and previous traumatic exposure. Considering these different pathways, it is hypothesized that the pivotal mechanism in disease origination and perpetuation differs between subjects, but it is not known how to differentiate between these subgroups of patients. Additionally, symptoms are often associated with lifestyle factors, such as diet, physical activity, and sleep. How these factors exactly relate to symptom patterns and potential underlying mechanisms, and how this association differs between subjects, is however unclear. In addition, apart from the known abdominal symptoms characteristic for IBS, these patients often also suffer from comorbid problems, such as psychological or physical non-GI symptoms as well as an altered stress response. Moreover, subgroups of patients can be truly diagnosed with comorbid disorders, such as anxiety disorders, depressive disorders, chronic fatigue syndrome, or fibromyalgia. This heterogeneity in comorbidities adds even more complexity to the already extensive differences in (GI) symptom presentation between subjects. Current knowledge on the etiology and pathophysiology of these overlapping syndromes is poor, and consensus on whether these syndromes do or do not share pathophysiological mechanisms is not yet reached.

The aim of the Discoverie project, which is a European multi-center collaboration in which 19 centers are participating, is to extensively characterize a large pan-European IBS cohort, considering clinical and biological outcomes, based on GI symptomatology as well as comorbid psychological/physical problems. This will help to get better insight in underlying pathophysiology and stratify patients to different (pathophysiological) IBS entities, and herewith leads the way to personalized care in the field of IBS. We at LaBGAS are primarily interested in uncovering the mechanisms of central nervous system function underlying mental and non-mental comorbidities of IBS.

Principal investigators
Lukas Van Oudenhove (LaBGAS), Ricard Farré (TARGID), Jan Tack (TARGID), Jeroen Raes (Raes Lab)
Team
Maaike Van Den Houte (LaBGAS), Lieselot Holvoet (TARGID), Alice Rustichelli (TARGID), Kristin Verbeke (TARGID)

From Pavlov to visceroception

Fear learning and the perception of visceral sensations The role of interoceptive fear conditioning in the development of fear of gastrointestinal symptoms, and its impact on perceptual habituation and discrimination of visceral sensations. Research Foundation - Flanders (FWO-Vlaanderen) research project granted to Ilse van Diest (Health Psychology), Lukas Van Oudenhove (LaBGAS) and Jonas Zaman (Health Psychology) · 2021-2025

As a cardinal symptom of most functional gastrointestinal disorders, visceral pain and discomfort are very common and disabling. Unfortunately, such symptoms remain poorly understood and are hard to treat. There is a general consensus that fear towards gastrointestinal sensations may play an important role, but the mechanisms underlying such fear as well as its impact on visceral symptom perception are unclear. The project aims to elucidate these mechanisms, building on our previous work demonstrating that fear of gastrointestinal sensations can be experimentally established through Pavlovian learning processes and that such fear learning changes the way persons perceive gastrointestinal stimuli. In healthy volunteers, we will investigate the effects of fear learning to an intitially non-painful gastrointestinal stimulus on different perceptual outcomes that are relevant for chronic visceral pain, including discrimination (the ability to discriminate slightly different stimuli) and habituation (decreased intensity perception upon repeated administration of an identical stimulus). These effects will be studied both at the self-report and the neural level (using electroencephalography). This project has the potential to dramatically increase our understanding of the relationship between learned fear of gastrointestinal symptoms and the occurrence of those symptoms. Such knowledge will foster the treatment of thus far "unexplained" gastro-intestinal discomfort and pain.

Principal investigators
Ilse Van Diest (Health Psychology), Lukas Van Oudenhove (LaBGAS), Jonas Zaman (Health Psychology)
Team
Lauren Pattyn (Health Psychology/LaBGAS), Livia Guadagnoli (LaBGAS)

Key publications

  • Zaman, J., Weltens, N., Ly, H. G., Struyf, D., Vlaeyen, J. W. S., Van den Bergh, O., Wiech, K., Van Oudenhove, L., & Van Diest, I. (2016). Influence of Interoceptive Fear Learning on Visceral Perception. Psychosomatic Medicine, 78(2), 248–258. https://doi.org/10.1097/PSY.0000000000000257
  • Ceunen, E., Zaman, J., Weltens, N., Sarafanova, E., Arijs, V., Vlaeyen, J. W. S., Van Oudenhove, L., & Van Diest, I. (2016). Learned Fear of Gastrointestinal Sensations in Healthy Adults. Clinical Gastroenterology and Hepatology : The Official Clinical Practice Journal of the American Gastroenterological Association, 14(11), 1552-1558.e2. https://doi.org/10.1016/j.cgh.2016.04.035

INBODY

Interoception across organ domains Whether interoception is a general ability with shared neural characteristics across the cardiovascular, respiratory and gastrointestinal systems, or a set of domain-specific capacities. Research Foundation - Flanders (FWO-Vlaanderen) and the Luxembourg National Research Fund (FNR) · 2021-2024

Functional somatic syndromes (FSS) are characterized by chronic, disabling symptoms that do not correspond to observable organic dysfunction. FSS are present across different organ domains (e.g. respiratory, gastrointestinal) and include diagnoses such as functional hyperventilation syndrome, irritable bowel syndrome, and functional heartburn. Treatment options for FSS are limited, which is largely due to insufficient knowledge about the mechanisms underlying these symptoms. Disturbed interoception, the ability to process and perceive sensory signals from within the body, is believed to be crucially involved. The INBODY project seeks to examine several important aspects of interoception in healthy individuals and patients with FSS. The project will examine interoception systematically at all stages of interoceptive signal processing (e.g., early neural processing, perception, and interpretation) across different organ systems in healthy individuals and patients with FSS. The primary aim is to investigate whether interoception is a general ability that shares neural processing characteristics across multiple organ domains and that predicts affective responses. We will also test whether altered interoceptive processing of bodily signals from different organs can explain the heterogeneity of somatic symptoms, especially in FSS, and how this can be modified by new treatment approaches. The INBODY project contains interrelated observational and experimental work packages that combine state-of-the-art methods including psychophysiological, neural and behavioural measures to improve the understanding of interoception within and across multiple organ domains and to establish interoception-based intervention strategies to reduce symptom burden in FSS patients.

Principal investigators
Nathalie Weltens (LaBGAS), Andreas von Leupoldt (Health Psychology), André Schulz (University of Luxembourg)
Team
Livia Guadagnoli (LaBGAS), Maaike Van Den Houte (LaBGAS)

Biopsychosocial mechanisms of chronic fatigue syndrome

Psychophysiology-based subgroups in ME/CFS Identifying (psycho)physiologically based subgroups in myalgic encephalomyelitis/chronic fatigue syndrome and testing their relevance for rehabilitation. Research Foundation - Flanders (FWO-Vlaanderen) · 2021-2024

About 20,000 people in Belgium suffer from Chronic Fatigue Syndrome (CFS), a disorder characterized by persistent fatigue insufficiently explained by known medical or psychiatric conditions. Dysfunction of several (psycho)physiological systems, such as the stress response system (including the hypothalamo-pituitary-adrenal axis and the autonomic nervous system), the immune system (systemic inflammation), and the central nervous system (including neuroinflammation and changes in functional connectivity in the brain) has been shown in CFS. Health psychology research, on the other hand, has demonstrated distortions in symptom perception in CFS. However, both research lines have not sufficiently been integrated, which is needed to overcome dualistic wars that have hampered progress in understanding and treating CFS. Specifically, it is poorly understood how the abovementioned dysfunctions relate to the experience of physical symptoms by CFS patients, particularly the perception of physical and mental fatigue. The aim of this project is therefore to investigate the complex relationships between fatigue perception and different psychophysiological dysfunctions in CFS patients, to identify subgroups based on these (psycho)physiological dysfunctions and relate these to rehabilitation success. This is urgently needed to develop a refined integrative pathophysiological model of this disabling though poorly understood disorder, for which treatment options are currently limited.

Principal investigators
Lukas Van Oudenhove (LaBGAS) and Katleen Bogaerts (REVAL, UHasselt)
Team
Maaike Van Den Houte (LaBGAS and REVAL, UHasselt), Omer Van den Bergh (Health Psychology), Stephan Claes (UPCKULeuven, Mind-Body Research), Elfi Vergaelen (UPCKULeuven)

SY-NAPS

The sleep-pain relationship Whether neuroinflammation mediates the bidirectional sleep-pain relationship, and the role of microglia in insomnia and chronic low back pain. Research Foundation - Flanders (FWO-Vlaanderen) research project granted to Iris Coppieters · 2023-2027

Chronic low back pain (CLBP) with and without insomnia is a highly prevalent and debilitating disorder characterized by huge socioeconomic burden. Sleep disturbances contribute significantly to CLBP severity and have a bidirectional relationship with chronic pain. This project will fill a critical knowledge gap by unraveling the underlying neurobiological brain mechanisms of this sleep-pain link in CLBP patients compared to pain-free controls with and without insomnia. We hypothesize that altered glial and neural brain mechanisms are linked to increased pain severity and sensitivity in response to acute and chronic sleep disruption. The effect of experimentally-induced acute insomnia will be studied with a randomized controlled crossover study in CLBP patients and pain-free controls. The impact of chronic sleep disturbances will be assessed via a cross-sectional case-control study in CLBP patients and pain-free controls with and without chronic insomnia. We will address our hypothesis by uniquely and ambitiously combining cutting-edge methods in neuroscience (PET-MRI to assess glial activation and neural responses to painful stimuli), pain (quantitative sensory testing to measure pain sensitivity and endogenous pain modulation), and sleep medicine research (ecologically valid sleep disturbance protocol and sleep assessments). Such research is urgently needed to develop effective and novel treatments for CLBP and insomnia that target the involved neurobiological mechanisms.

Principal investigators
Lukas Van Oudenhove, Iris Coppieters, Nathalie Weltens, Liesbet De Baets, Maarten Van Den Bossche
Team
Elin Johansson, Casper Vananderoye

Gut-immune-brain axis in IBD fatigue

Understanding fatigue in inflammatory bowel disease Whether the gut-immunity-brain axis holds the key to understanding persistent fatigue in inflammatory bowel disease. Category 1 internal KU Leuven funding, Research Foundation - Flanders (FWO-Vlaanderen) · 2024-2028

Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), is an inflammatory disorder of the gut, causing diarrhea, abdominal pain and blood loss. Fatigue is a common, debilitating comorbidity of IBD, severely impacting the QoL of IBD patients. Current anti-inflammatory treatments, used to alleviate the gastrointestinal symptoms, are inadequate in relieving fatigue symptoms, as 50% of IBD patients in remission still suffer from fatigue, indicating an urgent need to identify fatigue-related treatment targets. Although several possible causes have been identified, such as depression and sleep disturbance, the high prevalence of IBD-related fatigue is still unexplained, especially in remission. Emerging research has shown that fatigue, often present during acute inflammation as part of the sickness response, is a result of circulating pro-inflammatory proteins triggering neuroinflammation. Thus, we hypothesize that residual neuroinflammation, as a result of the mucosal-systemic-neuroinflammation cascade during active disease, is responsible for the persisting fatigue during remission. The aim of our study is to characterize the gut-immune-brain axis in IBD patients in a longitudinal study, where patients will be assessed during active disease and in remission. Inflammation will be assessed in the gut, systemic and brain, and correlated to fatigue, microbial composition, fecal short-chain fatty acid (SCFA) concentration and functioning of the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS). This will allow us to identify the inflammatory pathways that are involved in IBD-related fatigue, which could lead to new treatment targets.

Principal investigators
Bram Verstockt (IBD group), Maaike Van Den Houte (LaBGAS), Elfi Vergaelen (Mind-body Research), Lukas Van Oudenhove (LaBGAS)
Team
Sybren Rinckhout (LaBGAS and IBD Group) and Tuur Abts (LaBGAS and IBD Group)

Appetite & reward projects

Erythritol: satiation and reward without the calories?

A natural sweetener as an alternative to sugar Whether the natural non-caloric sweetener erythritol can replace sugar while preserving the satiating and rewarding properties of sweet taste, studied from gut hormone release through to brain reward responses. Research Foundation - Flanders (FWO-Vlaanderen) and the Swiss National Science Foundation (SNSF) · 2020-2023

Food intake is regulated by an intricate communication system between the gut and the brain. Hunger/satiety hormones released from the gut convey information on nutritional status of the body to homeostatic brain circuits sensing energy balance, but also influence reward system responses to food, hence its subjective pleasantness. Sweet is an innately attractive taste to humans because of the caloric value of carbohydrates, but sugar consumption is an important contributor to the obesity epidemic. Therefore, replacing sugar with artificial non-caloric sweeteners (NCS) has been proposed to reduce caloric intake and body weight. However, NCS may lack the satiating and rewarding properties of sugar because of their inability to influence the release of hunger/satiety hormones (in addition to lack of calories). The non-caloric natural sweetener erythritol may be an ideal alternative substitute for sugar, since we recently showed that it increases satiety hormone levels. Therefore, our aim is to study the effects of replacing sugar with erythritol (versus the artificial sweetener sucralose) on food intake regulation in healthy humans, and identify the (hormonal) gut-brain communication and brain mechanisms underlying these effects. This will generate much needed mechanistic-physiological knowledge, a necessary first step towards developing novel strategies for weight loss management and obesity prevention, and the role of NCS in general, and erythritol in particular, herein

Principal investigators
Lukas Van Oudenhove (LaBGAS), Anne Christin Meyer-Gerspach (St Clara Research & University of Basel, Switzerland)
Team
Aleksandra Budzinska (LaBGAS), Nathalie Weltens (LaBGAS), Fabienne Teysseire (St Clara Research/University of Basel)

Food reward after bariatric surgery

Dopamine and the endocannabinoid system in food reward Gut-brain mechanisms mediating the effects of bariatric surgery on food reward, investigated with PET-MR imaging of dopamine and endocannabinoid signalling. 2021-2025

Bariatric surgery (e.g., gastric bypass or sleeve gastrectomy) is currently the most effective method to induce significant and durable weight loss, which is mediated by caloric restriction, alterations in gut hormones, and eating behaviour (besides the decreased volume of the stomach). However, the neurochemical underpinnings of these effects remain poorly understood. The endocannabinoid (EC) and dopamine (DA) systems are key players in the regulation of food intake and energy balance, but how obesity and bariatric surgery affect EC and DA signaling both centrally and peripherally, and how this is related to altered metabolic hormone levels along the gut-brain axis remains unclear. The overall aim of this project is to gain fundamental insight in the interplay between the central and peripheral ECS and DA system and metabolic hormones before and after bariatric surgery, and their role in altered eating behaviour. To this end, we are conducting a longitudinal study in patients undergoing bariatric surgery in which we combine cutting-edge multimodal neuroimaging methods (PET, fMRI) with a set of innovative biochemical measurements (circulating and urinary EC and DA levels, metabolic hormones), and eating behaviour assessment. The results of this project may help pave the way for the development of novel, less invasive treatment options for obesity by identifying the neurochemical basis of the aberrant eating behaviour they should target.

Principal investigators
Roman Vangoitsenhoven (Clinical and Experimental Endocrinology), Nathalie Weltens (LaBGAS), Lukas Van Oudenhove (LaBGAS), Bart Van der Schueren (Clinical and Experimental Endocrinology)
Team
Nele Mattelaer (Clinical and Experimental Endocrinology, LaBGAS)

GLP-1 pharmacotherapy optimisation

Patient selection across the binge-eating spectrum A neuropsychobiological approach to improving the selection of patients for GLP-1-based pharmacotherapy for weight management across the binge-eating spectrum. Categorie 2 Maatschappelijk (C2M)-project · 2025-2029

GLP1-agonists including semaglutide have emerged as game changing drugs to support weight loss in obesity and are receiving increased attention for their potential role in treating maladaptive food reward behaviors, particularly binge eating (BE). However, how GLP1-agonists impact mechanisms regulating eating behavior and body weight loss is not well understood. Moreover, there is considerable variability in individual sensitivity to these drugs. Combined with the increasing demand for GLP1-based medications, this raises an urgent need for a more personalized treatment approach. Our aim is to improve patient selection for GLP1-based pharmacotherapy by investigating the impact of semaglutide on three distinct, but highly interacting motivational psychobiological processes crucial for changing individual eating behaviors and achieving weight loss in the treatment of obesity across the BE spectrum: i) gut-brain hunger/satiety signaling, ii) reward processing and its dopaminergic neural correlates and iii) emotional state.

Principal investigators
Roman Vangoitsenhoven (Clinical and Experimental Endocrinology), Nathalie Weltens (LaBGAS), Elske Vrieze (Mind Body Research), Lukas Van Oudenhove (LaBGAS), Bart Van der Schueren (Clinical and Experimental Endocrinology)
Team
Alexine Mennes (Clinical and Experimental Endocrinology and LaBGAS) and Annelies Falter (Clinical and Experimental Endocrinology and Mind Body Research)

Neuropsychobiology of human obesity

Study of the neuropsychobiological mechanisms underlying human obesity.

FWO — Research Project · 2026 – present

Microbiota & mind projects

GUTSIE

Short-chain fatty acids and executive function under stress Whether the gut bacterial metabolites known as short-chain fatty acids protect core executive functions against the effects of acute stress. United States Department of Defense - U.S Army Research Office · 2023-2025

The gut microbiome has emerged as a likely mediator of physiologic (e.g., hypothalamic-pituitary-adrenal (HPA) axis), emotional, and cognitive responses to stress. The short-chain fatty acids (SCFAs) acetate, propionate and butyrate are the main metabolites of fermentation of complex carbohydrates in the colon by the gut microbiota, and are thought to play a key role in microbiota-gut-brain communication. The effects of SCFAs on these communication pathways are likely via modulation of a combination of the following interacting mechanisms: decreasing inflammation, improving gut barrier integrity, inhibiting histone deacetylases, acting as ligands for G-protein coupled receptors, modulating vagal afferent signaling, crossing the blood-brain barrier, and modulating energy metabolism. In previous research from our lab, direct in vivo administration of SCFA to the large intestine of healthy humans, mimicking the effect of fiber fermentation, attenuated the cortisol response to acute stress. Previous findings suggest that a high cortisol response to acute laboratory stress in healthy participants is associated with long- and short-term negative effects, independent of changes in the subjective stress experience. On the long term, cohort studies indicate that a low cortisol response to acute laboratory stress is associated with a reduction in future health risks including but not limited to lower risk for development of a mental disorder (e.g., mood or anxiety disorders, and substance dependence disorders) and lower risk for developing hypertension. On the short-term, acute stress has been associated with modulation of cognitive functions. Most research in this area has been conducted in relation to core executive functions (higher cognitive processes that enable planning, forethought, and goal-directed action), revealing that acute stress and increased cortisol concentrations impair working memory (ability to keep information in mind and update/integrate current content with new information) and cognitive flexibility (refers to the ability to flexibly shift between cognitive rules or modes of thought), but enhance response inhibition (ability to inhibit proponent responses/actions in order to selectively engage with task-relevant information and goal-directed, rather than habitual behaviors). Building on these findings, the aim of the present proposal is to examine core executive function as a functional outcome of attenuating the cortisol response to acute laboratory stress through colonic delivery of an SCFA mix (acetate, propionate, butyrate).

Principal investigators
Lukas Van Oudenhove (LaBGAS), Kristin Verbeke (TARGID), Boushra Dalile (LaBGAS)
Team
Franco Ruiz

Short-chain fatty acids in anorexia nervosa

Microbial metabolites, stress responses and eating behaviour The psychobiological impact of undernutrition on cognition and emotion in anorexia nervosa, and the role of gut bacterial metabolites in regulating stress responses, eating behaviour and nutritional state. King Baudouin Foundation grant · 2021-2025

As a potent modulator of the bidirectional communication between the host's gastrointestinal tract and brain, the gut microbiota plays a central role in what's commonly known as the gut-brain axis. The gut microbiota can impact multiple bodily processes such as metabolism, immunological responses, body weight regulation, brain function, and eating behavior. In patients with anorexia nervosa (AN), who characteristically maintain highly restricted diets, significant alterations in gut microbiota composition have been reported. Moreover, shifts in the gut microbiota composition of patients with AN have been observed before and after renourishment. However, even after renourishment, the gut microbiota composition continues to differ from healthy controls.

Short-chain fatty acids (SCFAs), metabolites produced following the bacterial fermentation of dietary fiber in the large intestine, are considered candidate mediators of the gut bacteria's effects on the host. Acetate, propionate, and butyrate are the most abundant SCFAs and may affect the host through immune, endocrine, neural, and humoral pathways. In previous research from the lab, direct in vivo administration of SCFAs to the large intestine of healthy humans, mimicking the effect of fiber fermentation, attenuated the cortisol response to acute stress. Despite a growing body of evidence indicating a relationship between the gut microbiota and AN, there is a significant gap in research that causally examines the role of SCFAs and explores the interactions among the gut microbiota, SCFAs, stress response, and eating behavior in AN.

In this project, we will investigate the effects of short-chain fatty acids (SCFAs) as mediators of microbiota-gut-brain interactions on the acute stress response, eating behavior, and nutritional state in malnourished patients with anorexia nervosa (AN).

Quagebeur R, Dalile B, Raes J, Van Oudenhove L, Verbeke K, Vrieze E. The role of short-chain fatty acids (SCFAs) in regulating stress responses, eating behavior, and nutritional state in anorexia nervosa: protocol for a randomized controlled trial. J Eat Disord. 2023 Oct 26;11(1):191.

Principal investigators
Elske Vrieze (Mind Body Research group), Lukas Van Oudenhove (LaBGAS), Kristin Verbeke (TARGID)
Team
Robin Quagebeur (Mind Body Research group), Boushra Dalile (LaBGAS)

Methods

Our studies draw on a shared methodological toolkit:

  • Gut stimulation — intragastric and intraduodenal infusion of nutrients, fatty acids, bitter tastants and sweeteners; gastric and rectal barostat distension; oesophageal acid perfusion.
  • Brain imaging — task and resting-state fMRI, H₂¹⁵O and receptor PET (cannabinoid-1, opioid, dopamine), simultaneous PET-MR, and MR spectroscopy.
  • Psychophysiology — autonomic nervous system measures, cortisol and neuroendocrine stress responses, interoceptive accuracy paradigms.
  • Interventions — dietary challenges (FODMAP, gluten, sweeteners), probiotics and prebiotics, colonic short-chain fatty acid administration, pharmacological probes.
  • Analysis — multivariate pattern analysis, predictive modelling and brain signature approaches, built on CANlab tools and documented in our pipeline docs.

For the software behind the analyses, see Tools.