1. Terminology
This alphabetical glossary defines the guide's key scientific and clinical terms, so every word stays clear as you read.
This glossary defines the key scientific and clinical terms used throughout this guide. Terms are listed alphabetically. Terms marked (term used in this guide) are specific to this protocol.
The most abundant short-chain fatty acid produced by gut bacteria through fermentation. It serves as a metabolic substrate for both the host and other microbes. Its production reflects overall microbial fermentation activity.
Any unwanted or harmful effect that occurs during or after treatment. Adverse events can range from mild discomfort to severe complications. Monitoring adverse events is essential for FMT safety.
A measure of microbial species richness and evenness within a single sample. Higher alpha-diversity generally indicates a more resilient gut ecosystem. Common indices: Shannon entropy, Simpson's index, observed species count.
Microorganisms distinct from bacteria, some of which live in the human gut and contribute to metabolic processes such as methane production. They are a minor but relevant component of the gut ecosystem transferred during FMT.
A virus that infects and replicates within bacteria. Bacteriophages are present in the gut in enormous numbers and shape bacterial community composition. FMT transfers phages alongside bacteria, and phage engraftment may contribute to treatment durability. They are part of the broader microbial matrix transferred during FMT.
The patient's starting condition before treatment begins. It serves as the reference point against which later changes are measured. Accurate baseline assessment is essential for interpreting treatment outcomes.
A measure of microbial community differences between samples or individuals. High beta-diversity between donor and recipient before FMT does not predict outcome; post-FMT convergence toward donor beta-diversity is a marker of engraftment.
Molecules produced by the liver to aid fat digestion and then modified by gut bacteria into secondary bile acids. These microbial transformations influence metabolism and help suppress certain pathogens. Restoring bile acid conversion is one way FMT re-establishes ecological function.
A small, controlled exposure to donor microbiota used to observe the recipient's initial response before full treatment. It is conceptually similar to testing compatibility before full intervention, and forms the basis of the compatibility assessment process.
A short-chain fatty acid that serves as the primary energy source for colon cells. It supports the intestinal barrier and has anti-inflammatory effects in the gut. Restoring butyrate production is a key goal of FMT-supported recovery.
Oral administration of microbiota in encapsulated form. It allows repeated dosing over time and is less invasive than endoscopic delivery. It is especially useful in extended treatment protocols.
A prolonged and dysregulated inflammatory state associated with many metabolic, immune, and gastrointestinal conditions. Dysbiosis can contribute to its persistence by maintaining pro-inflammatory microbial signals.
The body's internal clock that regulates sleep, metabolism, and hormonal cycles. It also influences microbial activity and composition over a 24-hour cycle. Disruption of circadian rhythm can negatively affect microbiota stability.
Defined outcomes used to judge whether treatment is effective. These may include symptom improvement, remission, or specific biological markers. Clear endpoints help guide treatment decisions.
The capacity of the established gut microbiota to prevent the invasion and overgrowth of pathogens. FMT restores colonisation resistance primarily by re-establishing dense, diverse microbial populations that outcompete pathogenic species for nutrients and adhesion sites.
Delivery of donor microbiota directly into the colon using an endoscopic procedure. This method allows high-dose delivery in a single session and is often used when rapid, large-volume delivery is needed.
How well a donor microbiota interacts with a specific recipient's biological and ecological environment. It reflects immune response, metabolic interactions, and ecological fit. Variability in compatibility helps explain why patients respond differently to FMT from different donors.
A structured pre-treatment process used to evaluate how a recipient responds to different donor microbiota. It involves controlled exposure to donor material and monitoring of symptoms and physiological responses. Used in this protocol to inform donor selection before full treatment.
The process by which one group of organisms prevents another from occupying the same ecological niche. In the gut, beneficial microbes can suppress pathogens by outcompeting them for resources. FMT reintroduces communities capable of performing this function.
Phase 2 of the treatment protocol, during which repeated or sustained dosing supports microbial integration and stabilisation. The focus is on reinforcing changes initiated during induction and promoting ecological succession.
Plant-based carbohydrates that are not digested by human enzymes but are fermented by gut bacteria, producing metabolites such as SCFAs. Adequate fiber intake helps support microbial function and stability after FMT.
A healthy individual whose stool is used for FMT. Donors undergo extensive screening to reduce the risk of transmitting infections or other unwanted traits. Donor selection is a critical factor in treatment safety and effectiveness.
The process of evaluating potential donors for infectious, metabolic, and other health-related risks. It includes medical history, laboratory testing, and exclusion criteria. This process is essential for the safety of FMT.
Differences in microbial composition and function between donors. These differences can affect treatment response, because not all donor microbiota perform equally well in all recipients. Understanding donor variability helps explain why outcomes differ between patients.
The defined timing, frequency, and amount of microbiota administration. Different dosing schedules can influence ecological dynamics and treatment outcomes. Structured dosing is an important element of protocol design.
An imbalance in the composition, diversity, or functional capacity of the gut microbiota, associated with a range of clinical conditions. Dysbiosis may involve loss of beneficial species, overgrowth of pathogenic or pro-inflammatory taxa, reduced diversity, or disrupted metabolic output. It is not a disease in itself but an ecological imbalance. FMT is used to shift the system toward functional stability.
The role and functional position of a microorganism within an ecosystem, including the resources it uses, the conditions it requires, and its interactions with other species. FMT can restore balance by filling disrupted or unoccupied niches.
The ability of a microbial system to maintain its structure and function over time. Stable systems are more resistant to disruption and easier to maintain. A major goal of FMT treatment is to support long-term ecological stability.
The progressive change in microbial community composition over time following a disturbance, analogous to ecological succession in macro-ecosystems. Post-FMT, the gut undergoes a period of succession during which donor species compete with resident microbes for ecological niches.
The process of returning a disrupted microbial system to a more functional state. It involves rebuilding relationships and ecological functions, not merely adding organisms. This is the central conceptual model used in this guide to explain what FMT achieves.
The stable establishment of donor-derived microorganisms in the recipient gut following FMT. Engraftment is measured by comparing recipient microbiota composition before and after FMT to donor baseline. Partial and full engraftment are distinguished; clinical response does not always require complete engraftment.
Contact with external factors such as diet, chemicals, microbes, and physical conditions that continuously shape the microbiota and its activity. Changes in environmental exposure can affect the ecological conditions into which FMT is introduced.
A measure of how easily substances pass through the intestinal lining. Increased permeability is associated with inflammation and disease. Microbiota restoration may help support more normal barrier function.
A balanced and functionally stable microbial ecosystem. It supports digestion, immune regulation, and protection against harmful organisms. FMT aims to move the system toward this state.
The totality of environmental exposures an individual experiences throughout life and their cumulative biological effects. It includes diet, air quality, medications, stress, and microbial contacts. The exposome shapes microbial composition and is directly relevant to microbiota-based therapies.
A commensal bacterium of the Firmicutes phylum, consistently associated with gut health in human studies. It produces butyrate and has anti-inflammatory properties. Its abundance is frequently reduced in dysbiotic states and may be partially restored after FMT.
The transfer of a processed stool preparation from a healthy, screened donor into the gastrointestinal tract of a recipient. It delivers a complex microbial community with the aim of restoring disrupted ecological functions. It is the central therapeutic intervention described in this guide.
The process by which gut bacteria break down dietary fibers and other substrates in the absence of oxygen. This process produces metabolites such as SCFAs and is a core functional activity of a healthy gut microbiota.
A temporary worsening of symptoms in a chronic condition. It may be triggered by immune, environmental, or microbial changes. Recognising flares helps distinguish expected variability from clinical deterioration.
A structured tool for recording diet, symptoms, and related factors over time. It helps identify patterns and supports clinical interpretation of treatment response. In this guide, it is used as a key instrument for decision-making during FMT.
Microorganisms that form part of the gut ecosystem, collectively called the mycobiome. They interact with bacteria and the host in ways that may influence immune function and ecological balance. Their role in FMT is less well understood than that of bacteria.
The bidirectional communication network linking the gut microbiota, enteric nervous system, vagus nerve, immune system, and central nervous system. Microbial metabolites including SCFAs, tryptophan derivatives, and secondary bile acids modulate this axis. Changes in the microbiota may influence brain-related symptoms through this connection.
The dynamic relationship between the human body and its microbial community, including metabolic exchange, immune signalling, and structural interactions. FMT changes this relationship by introducing a new microbial system into the recipient's ecological environment.
The hypothalamic–pituitary–adrenal axis: the primary neuroendocrine stress-response system. Chronic activation of the HPA axis elevates cortisol, which alters gut motility, mucosal barrier integrity, and microbial composition. Dysbiosis itself can dysregulate HPA activity, creating a bidirectional stress-microbiota loop.
The influence of the microbiota on immune function through microbial metabolites and structural components. These signals help shape immune balance and responsiveness. FMT may improve gut health partly by restoring these microbial immune signals.
Communication between immune cells using chemical messengers. Microbial metabolites and structural components influence these signals, helping shape immune balance and responsiveness. Restoring microbial signals may be one mechanism through which FMT influences inflammation and immune tolerance.
The immune system's ability to avoid overreacting to harmless stimuli, including beneficial microbes. A healthy microbiota helps maintain this balance. FMT may influence tolerance by restoring appropriate microbial inputs.
Phase 1 of the treatment protocol, during which microbiota is introduced in higher doses. The goal is to initiate ecological change and begin restoration of key microbial functions. This is the first active treatment phase.
The body's response to injury, infection, or other threats. While necessary for protection, prolonged inflammation can contribute to disease. The microbiota plays an important role in shaping inflammatory processes.
Increased passage of microbial products (e.g., lipopolysaccharide) and other molecules through the gut epithelium into systemic circulation. This can activate innate immune responses and contribute to low-grade systemic inflammation. FMT may help restore barrier integrity through microbial and metabolic mechanisms.
Daily behaviours such as eating patterns, sleep, physical activity, and stress management that influence microbial growth conditions and metabolic activity. Optimising lifestyle factors can support the success of microbiota-based therapies.
The collection of small molecules produced by metabolic processes in the body and microbiota. These molecules mediate many interactions between microbes and the host. Changes in the metabolome reflect functional shifts after FMT.
A group of interacting microorganisms within a shared environment. In the gut, this community is shaped by cooperation and competition between species. FMT works by introducing a functioning community rather than single strains.
The variety of microbial species present within the microbiota. Higher diversity is generally associated with greater resilience and functional redundancy. FMT often aims to restore diversity as part of rebuilding ecological balance.
The microbiota viewed as an interconnected system of organisms, metabolites, and environmental conditions. It emphasises that function arises from relationships between species rather than isolated microbes. FMT targets this ecosystem as a whole.
The integrated system of microorganisms, metabolites, bacteriophages, and ecological interactions transferred during FMT. It emphasises that therapeutic effects arise from the structure and relationships within the community, not just its individual members. This term is used in this guide to describe the functional complexity of transplanted material.
The complete collection of microorganisms (bacteria, archaea, fungi, viruses, phages) and their genetic material in a defined environment. In clinical usage, 'gut microbiome' and 'gut microbiota' are often used interchangeably, though technically 'microbiome' includes the genes and 'microbiota' refers to the organisms. It describes not only which organisms are present, but what they do and how they influence physiological processes. In this guide, restoring the microbiome means restoring these functional processes rather than individual species.
The community of microorganisms (bacteria, archaea, fungi, viruses) inhabiting a specific environment. The human gut microbiota contains an estimated 10¹³ microorganisms representing thousands of species. In this guide, the microbiota is treated as a functional community that is directly modified through FMT, functioning as a network that carries out nutrient transformation, metabolite production, and immune interaction.
The broader therapeutic framework in which FMT is combined with targeted lifestyle and environmental interventions including diet, sleep, stress management, and other factors that influence microbial survival and integration. This is the term used in this guide for the full treatment model within which FMT is embedded.
The protective lining of the gut that separates the microbiota from the bloodstream, including mucus, epithelial cells, and immune components. A healthier microbiota supports maintenance of this barrier after FMT.
The absence of meaningful improvement after treatment. It may result from donor, recipient, ecological, or protocol-related factors. Identifying non-response is necessary for deciding whether treatment should be modified.
Incomplete but meaningful improvement after treatment. It suggests that some therapeutic effect has occurred, but not full resolution. Recognising partial response helps guide further clinical decisions.
The pre-treatment stage of the protocol, including preparation, compatibility assessment, and baseline evaluation. It defines the conditions under which treatment will begin.
The induction phase of treatment, during which microbiota is introduced in higher doses to initiate ecological change and begin restoration of key functions.
The consolidation phase, during which repeated or sustained dosing supports microbial integration and stabilisation of ecological changes.
The step-down or maintenance phase, during which intervention intensity is reduced while maintaining ecological stability and supporting long-term persistence of the restored microbiota.
A short-chain fatty acid produced by gut microbes and absorbed into the bloodstream. It is primarily processed in the liver, where it contributes to glucose regulation and systemic metabolic function. Shifts in propionate levels reflect changes in microbial activity after FMT.
The person receiving FMT. Their existing microbiota, immune system, and physiological state influence how the transplanted community behaves. Treatment outcomes depend on the interaction between donor and recipient factors.
A period during which symptoms are reduced or absent. It indicates clinical improvement, though not necessarily complete resolution of underlying causes. Sustained remission is one of the main goals of FMT treatment.
The ability of the microbiota to recover after disturbance. A resilient ecosystem can return to a functional state after stress such as antibiotic exposure or illness. FMT aims to improve this capacity.
A fermentable but slowly digestible form of starch that, in its raw state, behaves more like insoluble fibre. It acts as a prebiotic and is associated with broader ecosystem-level changes in the microbiota.
Measurable improvement after treatment, assessed through symptoms, clinical markers, or functional changes. Evaluating response guides decisions about whether the protocol is working as intended.
Metabolites produced by microbial fermentation of dietary fibre, primarily butyrate, propionate, and acetate. SCFAs are the main energy source for colonocytes, modulate mucosal immune function, and regulate intestinal barrier integrity. They are key markers of a functionally active microbiota.
The depth, duration, and regularity of sleep. Poor sleep can affect hormonal and immune pathways that influence the microbiota. Consistent sleep patterns may support microbial stability after treatment.
Phase 3 of the treatment protocol: the gradual reduction of intervention intensity after stabilisation. Its aim is to maintain therapeutic gains while allowing the microbial system to function more independently.
The body's physiological reaction to psychological or physical stress, involving hormonal changes that can alter gut motility, immune activity, and microbial composition. Chronic stress can work against stable FMT outcomes.
A donor whose FMT preparations consistently produce higher engraftment rates and better clinical outcomes across multiple recipients. The concept reflects observed variability in donor effectiveness but is not a standardised clinical definition.
Subjective experiences reported by the patient, such as pain, bloating, fatigue, or changes in bowel habits. They reflect how the body responds to underlying biological processes. Careful symptom tracking is essential for monitoring FMT response.
Protein complexes (including claudin, occludin, and ZO-1) that seal the spaces between intestinal epithelial cells. Their integrity is essential for preventing paracellular passage of bacteria and toxins. Dysbiosis-associated disruption of tight junctions contributes to epithelial permeability.
How well a patient can undergo treatment without significant adverse effects. It varies between individuals and protocols. Good tolerability supports adherence and continuation of therapy.
The systematic recording of symptoms, behaviours, or clinical observations over time. It helps reveal patterns that are not visible in isolated observations. Good tracking improves the quality of clinical decision-making.
A pattern of change observed over time. It helps distinguish temporary fluctuations from meaningful improvement or deterioration. Trends are more informative than single observations when evaluating treatment response.
An essential amino acid that serves as a precursor for serotonin (95% produced in the gut), the kynurenine[G] pathway metabolites, and indole[G] compounds. Gut bacteria regulate tryptophan availability and metabolic routing. FMT may influence mood, motility, and immune tone in part through restoration of tryptophan metabolism.
Fluctuations in symptoms or measurements over time. Some variability is expected, but excessive or irregular changes may indicate instability. Understanding variability helps interpret patient progress more accurately.
A nuclear receptor expressed in intestinal epithelial cells, immune cells, and other tissues. It regulates immune tolerance, epithelial barrier function, and microbial composition. Its activation is partially dependent on microbiota-derived secondary bile acids.
Symptoms that may indicate a serious or potentially dangerous development, requiring prompt attention and sometimes urgent medical review. Clear recognition of warning signs is a key component of safe FMT treatment.
A period during which no treatment is administered so earlier effects can diminish. It is used to separate treatment exposures or observe baseline conditions. In compatibility testing, washout helps isolate the response to a specific donor.
A protein that modulates the permeability of tight junctions in the intestinal epithelium. Elevated zonulin levels are associated with increased intestinal permeability. It is one measurable indicator of barrier dysfunction.