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See also: Gut Health In Brief
The microorganisms that live in our digestive tract play a prominent role in health and well-being. Although they can be found all along the digestive tract, the vast majority reside in the colon. Of all of these microorganisms, bacteria are the most studied. We provide a habitat for them; in return, they provide us with helpful compounds and functions (1).
The colon is an ecosystem densely populated with microbes (2). There is constant communication and interaction between microbes and host cells (3). Disturbances and imbalances can occur on either side of the relationship, which may contribute to the development of inflammation and other disease states (4).
While diet is not the sole determinant of the gut microbiota, its significance cannot be understated. Our dietary choices directly impact the abundance of particular bacterial species and the compounds they produce (5). Therefore, when considering our food choices, energy and nutrients for our bodies are not the only factors to consider, but also nurturing our gut microbiota.
The gut microbiota refers to the trillions of microbes — bacteria, yeast, archaea, and viruses — that live inside the gastrointestinal tract, mostly in the colon.
Bacteria are the most studied of these microorganisms. They reside all along the digestive tract, including the mouth, stomach, and throughout the small and large intestines. Their numbers increase as you move distally, and the vast majority inhabit the colon (Figure 1) (6).
The colon (1) stores undigested food mass; (2) absorbs water, nutrients, and electrolytes; and (3) provides a barrier against pathogens and harmful substances (7). The colonic barrier is composed of multiple barriers: (1) the gut microbiota (a biological barrier), (2) a mucus layer (a physical barrier), (3) an epithelial layer (a physical and chemical barrier), and (4) the immune system (an immunological barrier) (Figure 2) (8).
The mucus layer further consists of two layers: a loose, outer layer, containing gut microbiota members that can degrade carbohydrate structures (glycans) present on mucin; and a compact inner layer, largely devoid of bacteria (8-10). Maintenance of the mucus layer is very important — bacteria must be kept away from the colonic epithelium, otherwise an immune response may be activated, leading to inflammation (11, 12).
Viruses, fungi, archaea, yeasts, and many other microbes exist in the gut (4, 13). However, bacteria make up the majority of the biomass and diversity of the gut microbiota, are the most studied organisms, and are the focus of this article.
When we are born, we begin to be colonized by bacteria from our environment. Who stays and who goes is determined by many variables: genetic background; local exposures (such as family members, pets, and geographical location); external and lifestyle factors (such as medications and dietary choices); and microbial interactions within the colonic environment (between microbes and host cells as well as between each other) (4, 7, 14, 15).
Our first exposure comes from our mothers, starting with the mode of delivery (2, 15-17). Infants born by vaginal versus cesarean section birth have different initial gut microbiota compositions, reflecting their local exposures; this compositional variation decreases over time until it largely disappears by about three years of age (2). A series of progressive changes in the richness and diversity of the gut microbiota occurs over the first three years of life (2, 15). Early on, with a simple diet of human breast milk or formula, the infant gut microbiota is characterized by low diversity (2), and the factors present in these two diets select for different bacterial species during infancy. Human milk contains a high content of human milk oligosaccharides (HMOs), a type of indigestible carbohydrate (glycan), that is thought to guide the development of the infant gut microbiota by selectively feeding certain species, particularly members of the genus Bifidobacterium (18-22). HMOs also act as decoy molecules that bind pathogens, influence immune cells, provide building blocks, and stimulate intestinal barrier functions (18, 21). More than 200 unique HMOs have been identified in human milk; the structure and quantity of HMOs in human milk is highly variable, changing over the duration of lactation and influenced by the mother’s genetics (21, 22). Glycans attached to the colonic mucus layer may also have a role in early colonization by providing some bacteria with a source of endogenous nutrients (19). The gut microbiota of formula-fed infants is more diverse than that of breastfed infants, reflecting the differing substrates available to gut microbes (22). There is an ongoing effort to add HMOs and other characterized components of breast milk to infant formula (8, 21). Since 2016, two HMOs (2’-fucosyllactose [2’-FL] and lacto-N-neotretraose [LnNT]) have been successfully synthesized and approved for addition to infant formula in the United States and Europe (18, 21); their inclusion leads to a Bifidobacterium-dominated gut microbiota, which is typical of that observed in breastfed infants (21, 22). The European Food Safety Authority (EFSA) has also approved the addition of other synthetic oligosaccharides, such as lacto-N-tetraose (LNT), 2’-FL + difucosyllactose (DFL), 3’-sialyllactose (3’-SL), and 6’-sialyllactose (6’-SL) (23). While there are no safety concerns regarding the addition of these approved synthetic oligosaccharides to infant formula, no firm conclusions about clinically relevant benefits can be made at this time (23).
The introduction of solid foods along with the cessation of breastfeeding initiates a marked increase in complexity and diversity of the infant’s gut microbiota (2, 7, 16, 24, 25). The more complex and diverse diet leads to a shift in bacterial metabolism and crossfeeding between species, paving the way for successive colonization events (24). Transitions are induced by the establishment of an anaerobic environment, altered nutrient availability, and microbial interactions during community succession (24).
Bacterial composition continues to diversify over time until it stabilizes into a mature microbiota during the teen years (15), with trillions of bacteria inhabiting our gut. Bacterial populations fluctuate in abundance depending on changing internal and external variables, but the gut microbiota eventually returns to this established baseline (4). Although we each have our own unique mixture of bacteria, these many different bacterial species fall into five main groups (Figure 3) and share some broad functions (see Functions).
The microbiome refers to the genetic content of the gut microbiota. It consists of several million genes (in comparison, the human genome contains about 20,000 genes) that encode proteins and functions that complement or are otherwise not present in the host (26). Additionally, different species of bacteria may possess some of the same genes; thus, even when the specific taxa present differ between individuals, the gut microbiome may encode shared, core functions (27).
The bacteria in the gut affect the host in many ways; a couple of these functions include (1) protection against pathogens, and (2) production of beneficial compounds.
Protection against pathogens. In a healthy gut microbiota, a higher abundance of beneficial bacterial species (commensals) inhibit the growth of pathogenic species, a phenomenon known as colonization resistance (1, 28). Commensals use several strategies to prevent pathogen outgrowth, including limitation of space and nutrients, production of toxic substances, changing pH and oxygen levels, supporting the colonic mucus layer, and induction of the host immune response (1, 7, 9).
Colonization resistance can be distressed and turn ineffective — due to host factors, diet, infection, or medication usage, for example — leading to an outgrowth of opportunistic bacterial species that are typically kept in check by commensals.
Production of beneficial compounds. A variety of compounds are produced by commensal microbes in the colon, including vitamins (vitamin K, and several from the vitamin B family), fermentation products, hormones, neurotransmitters, gases (carbon dioxide, methane, hydrogen sulfide, hydrogen gas), and many other small molecules and metabolites (see Gut Microbiota Metabolites) (29-31).
These compounds exert both local and systemic effects. Locally, bacterially-produced compounds nourish the cells of the colonic epithelium and help maintain the integrity of its protective mucus layer (7, 12). Colonic endocrine cells (L cells) express receptors that are activated by various bacterial metabolites, inducing the secretion of key gut peptides and hormones (see Gut Microbiota Metabolites) (32). In addition to helping host cells, commensals cultivate the growth of other beneficial microbes through the exchange of nutrients and other compounds (a process called syntropy) (19, 28). Systemically, bacteria-derived compounds can be absorbed into the bloodstream and lymph, where they travel to other parts of the body (28). Metabolites can interact with cellular receptors — in the liver, brown and white adipose tissue, skeletal muscle, blood vessels, and central nervous system — to activate or inhibit signaling pathways, thereby influencing host health (7, 32).
The composition of a normal, average, healthy adult gut microbiota has not been defined. However, it is generally dominated by obligate anaerobic bacteria (14, 32) and characterized by high diversity (1).
Commensals versus pathogens. In a healthy host, gut commensals are dominant over pathobionts (bacterial species that become pathogenic under certain conditions) (1). Most commensal bacteria are obligate anaerobes (9). They like certain substrates (especially non-digestible carbohydrates [NDCs] from a diversity of plants), low pH, and anoxic conditions. Meeting these criteria helps commensals thrive and outcompete pathogens and pathobionts.
Pathogens and pathobionts are mostly facultative anaerobes; their numbers are usually kept in check by commensals (1). Pathogens use a variety of strategies to stick around and gain a growth advantage over commensals: they express unique metabolic pathways that are absent in commensals, most produce toxins that induce gut inflammation, and they themselves benefit from inflammation (1).
Microbiota diversity. A community that contains many species (i.e., high in diversity) is more stable and resilient in the face of a perturbation (3, 4). The gut microbiota faces external challenges daily — some are brief and some are continuous. Examples include changes in dietary patterns, infection with a pathogen, and medication use (especially antibiotics) (3, 4).
A diversity of bacterial species not only provides a diversity of functions but also results in an increased level of functional redundancy, meaning that some bacteria can compensate for the loss of a beneficial strain, providing functions and metabolites that may be otherwise lost in the face of a perturbation (4, 33). As a result, the gut microbiota can recover to the state that existed before the perturbation, a phenomenon known as resilience (3, 4).
Certain dietary patterns and lifestyle factors are associated with increased diversity (see Dietary patterns), while multiple disease states are associated with a decrease in the diversity of the gut microbiota (1, 34).
While the small intestine is very efficient at digesting and absorbing nutrients, some food material is either indigestible (humans lack the enzymes required to break it down) or escapes digestion and reaches the large intestine (32). This indigestible and undigested material is what becomes substrate for gut microbes.
Classes of substrates that make it to the colon include indigestible complex carbohydrates (such as fiber and glycans), some proteins and amino acids, bile acids, and phytochemicals. Bacterial enzymes act upon this undigested material, leading to the production of a variety of small molecules, or metabolites. Microbial metabolites exert their influence both inside the gut and in other parts of the body, since they can be absorbed by the host and travel to other body sites by way of the blood and lymph (32).
Microbial metabolites can have direct effects, used as energy substrates or essential cofactors, and indirect effects, whereby they interact with different host receptors and engage a number of cellular signaling pathways (27, 28).
Dietary fiber is a diverse group of non-digestible carbohydrates (NDCs) that can be found intrinsic and intact in plants (see the article on Fiber) or may be isolated or chemically synthesized (FDA fiber definition). Commensal bacteria love soluble dietary fiber, and bacterial fermentation of soluble fiber yields short-chain fatty acids (SCFAs). The main SCFAs produced are acetate, propionate, and butyrate, though many others are produced, such as formate, lactate, and succinate (31). Their proportion in the colon varies by diet (you must provide the substrate) and microbiota composition (bacterial species able to produce the SCFA must be present) (34, 35).
Much research has focused on butyrate, which has a principal role in intestinal barrier function and colonization resistance. Butyrate achieves this by several mechanisms (4, 9, 27, 28, 32, 36):
Maintenance of colonic barrier function alone is a critically important role for SCFA-producing bacteria. Still, SCFAs exert additional beneficial effects both inside the colon and at a distance, as signaling molecules and as substrates incorporated into glucose and lipid metabolic pathways (7, 27, 36, 37). For example, SCFAs bind G-protein coupled receptors (GPCRs) that are expressed at the surface of colonic endocrine cells (L cells) and a wide-range of tissues and cell types throughout the body (32). In colonic L cells, SCFA interaction with GPCRs stimulates the secretion of gut peptides (GLP-1, GLP-2, and peptide YY) that can improve glucose-stimulated insulin secretion, reduce appetite, and slow down intestinal transit (7). SCFAs that are absorbed into the circulation, especially acetate and propionate, are oxidized in the liver and skeletal muscle and may play a role in appetite regulation (7, 36, 37). Additionally, many intestinal inflammatory diseases are associated with a reduced abundance of bacterial species that produce SCFAs (4, 32, 35).
Depending on their level of intake or chemical structure, some dietary proteins escape digestion and reach the large intestine (6, 32). Additionally, proteins derived from the turnover of sloughed off intestinal cells and their contents become substrates for gut microbes. Protein fermentation results in the production of ammonia, amines, N-nitroso compounds, phenolic and indolic compounds, and branched-chain amino acids (6). Some microbial metabolites produced from proteins are beneficial, others are detrimental.
From tryptophan, gut microbes can produce indole or indole derivatives (27, 28, 35). Indoles interact with the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that induces genes involved in recovery from inflammation, xenobiotic metabolism, protection against pathogen colonization, and barrier function (35). From glutamate, gut microbes can produce γ-aminobutyric acid (GABA), a neurotransmitter involved in the mediation of pain in the intestine and with the regulation of mood in the central nervous system (28).
Fermentation of certain dietary factors produces compounds that can be toxic (4). Bacterial fermentation of dietary choline, phosphatidylcholine, carnitine, and betaine produces a compound known as trimethylamine (TMA) (34, 38, 39). TMA travels to the liver where it is enzymatically converted to trimethylamine-N-oxide (TMAO). TMAO circulates in the plasma and is normally efficiently excreted by the kidneys (40). However, elevated plasma TMAO has been associated with an increased risk of atherosclerosis and cardiovascular disease (38, 39), possibly by increasing macrophage cholesterol accumulation and foam cell formation (see the article on Choline) (39).
Notably, one’s bacterial community could impact the amount of TMAO that is produced upon exposure to its dietary precursors (found in red meat, eggs, and fish) (38, 41). Certain species of bacteria must be present to produce TMA (34, 38), and the presence of bacterial species that consume, detoxify, or convert TMA into a beneficial signal can also vary from person to person (32). Ultimately, plasma levels of TMAO are determined by many variables: the dietary source of its precursor, the gut microbiota, kidney function, and likely many other host factors.
Bile acids aid in the digestion and absorption of dietary fat. Approximately 95% of intestinal bile acids are reabsorbed in the ileum of the small intestine and return to the liver for re-secretion. Only a small fraction of bile acids escape this highly efficient loop and reach the colon (32, 35). These primary bile acids are modified by gut microbes, resulting in the formation of secondary bile acids. Deoxycholic acid, lithocholic acid, and ursodeoxycholic acid are the most common secondary bile acids (32, 35), but hundreds more exist (27).
Secondary bile acids help to inhibit inflammation and pathogen overgrowth (35). Some mechanisms of action include (1) binding farnesoid X receptor (FXR), a ligand-activated transcription factor that induces the expression of antimicrobial peptides and inhibits the pro-inflammatory transcription factor NF-κB; (2) binding transmembrane G-protein coupled receptors (GPCRs) at the colonocyte surface, thereby inducing signal transduction cascades that enhance tight junctions; and (3) direct antimicrobial effects by damaging pathogen membrane integrity (35, 42).
However, depending on their concentration, level of hydrophobicity, and conjugation status, secondary bile acids can exert negative, cell-damaging effects to host cells in the liver and gastrointestinal tract (43). As a result, a connection between secondary bile acids with inflammatory bowel disease, nonalcoholic fatty liver disease, and cancers of the liver, esophagus, and colorectum has been observed, although the potential role of bile acids in the establishment and progression of these diseases is still being investigated (43).
Phytochemicals are chemicals from plants that may benefit health (see the articles on Phytochemicals). They encompass a very large, diverse group of chemical compounds, and hundreds of phytochemicals can exist in a single food.
One class of phytochemicals, polyphenols, is known for its broad anti-inflammatory and antioxidant effects through their modulation of cellular signaling pathways and transcription factors (see the article on Flavonoids) (35). Members of this class include flavonoids, phenolic acids, lignans, stilbenes, curcuminoids, coumarins, and tannins (35). Many dietary polyphenols are poorly absorbed, which limits their interaction with target tissues; however, polyphenols that remain in the intestinal lumen can reach the colon and interact with gut microbes (35).
Bacterial species from four of the dominant phyla (Bacillota, Bacteroidota, Actinomycetota, and Pseudomonadota; Figure 3) possess enzymes that metabolize phytochemicals (44). Enzymatic reactions, such as deglycosylation, demethylation, dehydroxylation, isomerization, and decarboxylation, transform the parent polyphenol into a number of derivatives (35, 44).
Based mainly on in vitro and animal studies, polyphenol metabolites may exert several beneficial effects in the gut: (1) they selectively encourage the growth of beneficial bacteria (i.e., have a prebiotic effect); (2) they exert an antimicrobial effect specifically against pathogenic microbes (through adherence to cell wells, binding of DNA replication factors, disruption of biofilms, and chelation of essential nutrients); and (3) they inhibit NF-κB, a ubiquitously expressed transcription factor that induces a number of pro-inflammatory genes (35).
However, large variability exists between individuals. Specific bacterial species must be present in order to generate breakdown products from different phytochemicals (44, 45), therefore, individual differences in gut microbiota composition can influence the form and amount of phytochemical derivative that is produced. Inside colonic and liver cells, phytochemical metabolites encounter the cytochrome P450 (CYP) family of enzymes, which mediate phase I and II transformation reactions (45). There is a great deal of genetic variability in CYP family enzymatic activity, ranging from nonfunctional to increased function, representing another layer of complexity (45).
What we eat influences the abundance and activity of the microbes that live in our gut.
Composition/abundance. Bacterial abundance changes rapidly in response to extreme dietary changes. For example, in a human study, within two days of eating an entirely animal-based diet nearly devoid of dietary fiber versus a plant-based experimental diet that provided over two times the Adequate Intake (AI) for fiber, microbial composition was altered such that certain clusters of bacteria characterized each dietary pattern (46). Upon withdrawal of the experimental diet, the microbial composition reverted back to its baseline state just as quickly (46). The same is true for other dietary interventions, for example the addition of >30 g/day of specific dietary fibers (47) or following a high- or low-fiber diet for 10 days (48). Overall, one must constantly provide the dietary substrate to maintain the altered microbiota composition (5, 49).
Metabolites produced/metabolome. In addition to influencing the growth and proliferation of bacteria, dietary substrates strongly affect what these bacteria produce. The collection of small compounds produced by the gut microbiota is called the metabolome.
There are two main observations regarding the influence of diet on the production of bacterial metabolites. First, even though bacterial composition may not change in response to a dietary intervention, the metabolites produced might change (50). Secondly, delivery of substrate is necessary, but not sufficient, to control metabolite production; in other words, certain bacteria must be present in order to produce certain metabolites (34). Some individuals may have a ‘restrictive’ community structure, meaning that they cannot produce certain metabolites even when specific foods are consumed. For example, some individuals were not capable of increasing production of SCFAs when supplemented with fermentable carbohydrates (34). The same has been observed for the production of equol following soy isoflavone consumption (see the article on Soy Isoflavones). This may be due to the absence of certain species of bacteria whose activities are required to degrade a given substrate (34).
Thus, both dietary substrates and the gut microbes present are determinants of which metabolites are produced.
Dietary patterns. Several observational studies report that long-term consumption of plant-based diets is associated with greater bacterial diversity and higher levels of SCFA production (5, 31, 34, 51). Regular consumption of plant foods has been associated with a higher abundance of commensals, while consumption of processed foods and animal-derived foods (with the exception of fish) is associated with a higher abundance of opportunistic bacteria (52). Furthermore, a diverse diet, and in particular, the number of different types of plant foods consumed, has been associated with greater microbial diversity (5, 53). Following the recommendations in the Dietary Guidelines for Americans is also associated with higher microbial diversity and enrichment of microbes capable of fiber degradation (54).
Non-digestible carbohydrates (NDCs) figure prominently in the host-gut microbiota relationship. A vast array of dietary carbohydrates resist digestion in the human small intestine, either because humans lack the enzymes necessary to break down or cannot gain access to their internal chemical bonds (see the article on Fiber). The gut microbiota, on the other hand, expresses thousands of carbohydrate-active enzymes (CAZymes) capable of targeting a wide range of complex carbohydrates (20, 31). NDCs escape digestion in the small intestine and reach the large intestine, becoming primary substrates for the gut microbiota. Soluble fiber, glycans, and resistant starches fall into this large category of NDCs — they have slightly different types of linkages between their component sugar molecules giving them distinct conformations, yet all of them are important substrates for fermentation by the gut microbiota.
Low NDC intake reduces the production of SCFAs and shifts the gut microbiota metabolism to use less favorable nutrients, including glycans from the colonic mucus layer (51). Accumulating evidence indicates that a Western-style diet (low fiber; high saturated fat, sugar, and processed foods) degrades the colonic mucus barrier, contributing to pathogen susceptibility and inflammation (10, 11, 31, 51, 55).
Overall, a diet rich in non-digestible carbohydrates (fermentable fiber, glycans, and resistant starch; see the article on Fiber), with adequate intake of macro- and micronutrients, and a diversity of plant foods is associated with higher gut microbial diversity and considered beneficial for health (4, 5, 31). Long-term, habitual dietary change is required to influence the abundance and functional output of the gut microbiota (5, 49).
Probiotics are live microorganisms that, when administered in adequate amounts, confer a health benefit on the host (56). Many cultured dairy products contain probiotics; other sources include some fermented foods and dietary supplements. Processing can impact the quantity of live microorganisms as cooking and heating can destroy some microorganisms.
Commercially available probiotics typically provide lactobacilli or bifidobacteria, but more and more bacterial species are being characterized as potential probiotic candidates (27, 57). Keep in mind that these bacteria typically stay in the gut temporarily, making regular consumption necessary.
Probiotic effects are strain and dose dependent (56). A strain is a group of organisms that belong to the same species but share certain genetic characteristics not found in other members of the same species. The effective dose has been determined through clinical trials and reflects the number of live microbes present through the end of a product’s shelf life (58). Because of this specificity, products should be labeled with the genus, species, strain, and effective dose of any probiotic contained therein (see the infographic from the International Scientific Association for Probiotics and Prebiotics).
Cell culture, tissue extracts, animal models, and human studies demonstrate that probiotics act through a variety of mechanisms, such as modulation of immune function; antagonism against pathogens (through reduction of pathogen adhesion and aggregation, competition for nutrients and host cell binding sites, and production of antimicrobial compounds); production of beneficial metabolites; changes in the local environment (i.e., pH lowering); and provision of enzymatic functions (57, 59, 60).
Many different benefits have been associated with different probiotic strains; to access those benefits, the specific strains at the specific doses should be used (58, 61). Aggregate data from systematic reviews and meta-analyses of clinical trials have suggested that probiotics might be effective for several clinically relevant endpoints, such as treating acute diarrhea, reducing the incidence of antibiotic-associated and C. difficile diarrhea, treating colic in breastfed infants, and managing symptoms of lactose intolerance, among other conditions (58). Moderate scientific evidence exists for the use of probiotics along with antibiotic therapy to reduce the duration of antibiotic-associated diarrhea in adults (62) and children (63). However, in general, there is not adequate evidence to suggest that normal, healthy adults should take probiotics daily (64).
Many variables influence the probiotic response and impact: individual differences (such as health status, baseline microbiota, genetic background); the presence of cooperative species or combinations that may be needed as bacteria work together (syntrophy); and the coadministration of a prebiotic (60). Additionally, safety in vulnerable populations (those with chronic diseases or critical illness, the immunocompromised, and preterm infants) should be considered before adding a probiotic (65, 66).
Foods containing live and active cultures. Foods that contain high levels of live and active cultures are usually fermented. Although not all fermented foods retain live microbes when consumed (e.g., sourdough bread), even the fermented foods that retain live microbes do not necessarily qualify as probiotics (67). A probiotic must be identified to the strain level, must have been tested in controlled human studies to demonstrate a health benefit, and must be administered at the dose shown to be effective. No general dose can be specified for all probiotics; different doses may be needed for different health benefits (56). In the case of fermented foods, the microbes may not be defined to the strain level and may not have been shown to confer a health benefit.
Higher consumption of foods containing live microbes (including from fermented foods [see the article: Gut Health In Brief Health]) is associated with modest health improvements across a range of outcomes (systolic blood pressure, C-reactive protein, plasma glucose, plasma insulin, triglycerides, HDL cholesterol, waist circumference, and body mass index) (68). That said, food is a complex mixture of substances, and it is not possible to clearly distinguish the contribution of the live microbes from that of the food matrix, macro- and micronutrients, and other dietary factors (68, 69). Still, an update to the dietary guidelines with the daily inclusion of foods containing safe, live microbes is a topic of consideration (70).
A prebiotic is a substrate that is selectively utilized by host microorganisms, conferring a health benefit (71). Prebiotics promote the growth and metabolic activity of specific, beneficial gut microbes, which includes both administered probiotics and resident bacteria (57, 71).
Prebiotics include certain soluble fibers, such as oligofructose, inulin and fructooligosaccharides. Several additional substances are being researched as prebiotics, including glycans, resistant starch, phytochemicals, polyunsaturated fatty acids, conjugated fatty acids, and oligosaccharides (71). Non-digestible carbohydrates (NDCs) are the main substrate for microbial growth in the colon (4). When NDCs are limited, bacteria can turn to alternative energy sources from the diet, or may degrade host glycans present in the gut mucus layer (4, 19).
The two compounds most extensively tested and with confirmed prebiotic effects are inulin-type fructans (ITF) and galacto-oligosaccharides (GOS) (60, 71). Both ITF and GOS selectively increase the numbers of bifidobacteria and lactobacilli, bacterial groups that are also available as probiotics (31). ITF occur naturally in several foods, such as leek, asparagus, artichoke, garlic, onion, chicory, wheat bran, green banana, and soybean. Legumes and pulses are good sources of GOS. In general, consuming a diversity of plant foods is likely to provide a variety of prebiotic compounds.
As with probiotics, the influence of a prebiotic ingredient on the gut microbiota is transient. Changes in microbial composition respond rapidly — within 24 hours of exposure — and disappear equally fast upon withdrawal of the prebiotic compound (51). Additionally, response to a prebiotic is highly individualized (34, 51) and dependent on the initial gut microbiota composition (31).
Postbiotics are preparations of inanimate microorganisms and/or their components that confer a health benefit on the host (72). Postbiotics must contain inactivated microbial cells or cell components, and may or may not contain the microbial metabolites generated during the growth of the progenitor microbe(s) (72).
A role for non-live bacterial components has been documented in animal and in vitro models (27): a thermostable outermembrane protein from Akkermansia muciniphilia improves gut barrier function in mice (73); supernatants from A. muciniphilia bacterial cultures have anti-inflammatory potential in vitro (74); and heat-killed Lacticaseibacillus paracasei influences cytokine secretion by immune cells in vitro (75). Health effects of postbiotics appear to operate through mechanisms that are characteristic of probiotics (76), but of course metabolic activity, as well as other mechanisms requiring activity of the cell, is not possible with a postbiotic. Mechanisms of action include modulation of resident microbes, enhancement of epithelial barrier functions, modulation of local and systemic immune responses, modulation of systemic metabolic responses, and systemic signaling via the nervous system (72, 76).
Overall, postbiotics seem to mimic some of the beneficial effects of probiotics, while possibly avoiding the risk of administering live microorganisms to vulnerable populations (76-78). However, although an infectious nature of a postbiotic is not a concern, postbiotics must be assessed for safety, just as any bioactive agent would be. Research into the efficacy of these products is only just beginning.
The composition of the average healthy gut microbiota has not yet been defined. However, features of a healthy microbiota include diversity and a dominance of commensal species (obligate anaerobic bacteria). Your dietary and lifestyle choices impact which bacterial species thrive and what they produce. This in turn influences the health of the colon and other organ systems.
When deciding what to eat, it’s not just about energy and nutrients for your body; it’s also about what you are feeding your gut microbiota. Regardless of your background composition, the same guiding principles apply:
As we learn more about the microbiota, the guidelines may expand. For example, the daily inclusion of foods with safe, live microbes (such as fermented foods) or personalized recommendations based on one’s microbiota composition may become possible (31, 40, 70). As we await more scientific information, the good news is that following the existing dietary guidelines establishes a framework that is good for both your body and the microscopic organisms with which it coexists.
Written in May 2024 by:
Giana Angelo, Ph.D.
Linus Pauling Institute
Oregon State University
Reviewed in July 2024 by:
Mary Ellen Sanders, Ph.D.
Mary Ellen Sanders, LLC
Probiotics Consulting
Centennial, CO
Reviewed in October 2024 by:
Hannah D. Holscher, Ph.D., R.D.
Associate Professor of Nutrition
University of Illinois Urbana-Champaign
This article was underwritten, in part, by a grant from Amway.
Copyright 2024-2025 Linus Pauling Institute
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