Metabolism and gut health -
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Ussar S, Griffin NW, Bezy O, Fujisaka S, Vienberg S, Softic S, et al. Interactions between gut microbiota, host genetics and diet modulate the predisposition to obesity and metabolic syndrome. Download references. CLB had a PhD scholarship funded by Nestlé RDLS and is currently funded by Metabometrix Ltd.
Metabometrix Ltd, Bio-incubator, Prince Consort Road, South Kensington, London, SW7 2BP, UK. Division of Computational and Systems Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Sir Alexander Fleming Building, Exhibition Road, South Kensington, London, SW7 2PH, UK.
Ana Luisa Neves, Julien Chilloux, Jeremy K. You can also search for this author in PubMed Google Scholar. Correspondence to Jeremy K. Nicholson or Marc-Emmanuel Dumas. CLB, ALN, JC, and M-ED were involved in drafting the manuscript. CLB, ALN, JC, M-ED, and JKN were involved in critically revising the manuscript for the intellectual content.
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Boulangé, C. et al. Impact of the gut microbiota on inflammation, obesity, and metabolic disease. Genome Med 8 , 42 Download citation. Published : 20 April Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article.
Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Review Open access Published: 20 April Impact of the gut microbiota on inflammation, obesity, and metabolic disease Claire L.
Boulangé 1 , Ana Luisa Neves 2 , Julien Chilloux 2 , Jeremy K. Abstract The human gut harbors more than trillion microbial cells, which have an essential role in human metabolic regulation via their symbiotic interactions with the host.
Full size image. Obesity and the metabolic syndrome Obesity is characterized by an excess of adipose tissue and occurs when an imbalance exists between energy intake and energy expenditure [ 14 ]. Link between impaired insulin action, low-grade inflammation, and obesity In healthy individuals, insulin triggers glucose uptake in peripheral organs and the secretion of this hormone is activated by the rise in postprandial plasma glucose concentration.
Interactions between gut microbes and host metabolism in the physiopathology of obesity and the metabolic syndrome Although genetic variants have been associated with susceptibility to developing obesity and type 2 diabetes, the heritability of these variants is fairly modest.
The gut microbiota affects calorie harvest and energy homeostasis A body of evidence shows that the gut microbiota helps to harvest energy and increase host fat storage [ 33 , 34 ]. Therapeutic potential of manipulating the gut microbial ecology The study of the metabolic, signaling, and immune interactions between gut microbes and the host, and how these interactions modulate host brain, muscle, liver and gut functions, has raised the concept of therapeutic microbial manipulation to combat or prevent diseases [ 4 , 10 ].
Conclusions and future directions The evidence for a strong contribution of the gut microbiota to the onset of obesity and metabolic diseases is growing. References Bruzzese E, Volpicelli M, Squaglia M, Tartaglione A, Guarino A.
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Google Scholar Piya MK, McTernan PG, Kumar S. The utilization of these substrates is mainly the result of cross-feeding between gut microbiota members, rather than host absorption. Three main strategies for this activity exist in the human gut: 1 acetogens, for example, Blautia spp.
A higher abundance of these cross-feeders may improve the overall efficiency of metabolism in the gut; for example, an increase in methanogens is observed in the GI tract of anorexia nervosa patients, which may be a coping strategy by the gut microbiota in response to a lack of food sources [ 78 , 79 ].
Sulfate-reducing bacteria are the most efficient of the hydrogenotrophs, but require a source of sulfate; in the gut, the most prominent source of sulfate is sulfated glycans [ 80 ]. Although some of these glycans may be obtained from the diet, the most accessible source is mucin produced by the host [ 38 ].
Sulfate-reducing bacteria obtain sulfate from these substrates via cross-feeding with microbes such as Bacteroides , which produce sulfatases [ 80 , 81 ].
Hydrogen sulfide is both directly toxic to IECs through inhibition of mitochondrial cytochrome C oxidase, and pro-inflammatory via activation of T helper 17 cells [ 82 , 83 ]. Hydrogen sulfide can additionally directly act on disulfide bonds in mucin to further facilitate mucin degradation [ 84 ].
Elevated hydrogen sulfide concentrations and increased proportions of sulfate-reducing bacteria are reported in IBD [ 85 ]. The digestibility of proteins by the host is more variable than that of carbohydrates and fats, and is influenced by the previously mentioned factors of food processing, macronutrient ratios, and transit time [ 14 , 18 ], in addition to its source e.
The extra steps of interconversion required for amino acid fermentation yield a large diversity of by-products. However, it is important to note that not all amino acids are fermented to toxic products as a result of gut microbial activity; in fact, the most abundant end products are SCFAs [ 13 , 14 ].
Therefore, it may not be protein catabolism per se that negatively impacts the host, but instead specific metabolisms or overall increased protein fermentation activity.
It is thus important to examine these subtleties. A microbe can exhibit one of two strategies for the initial step of amino acid catabolism, either deamination to produce a carboxylic acid plus ammonia or decarboxylation to produce an amine plus carbon dioxide [ 12 ].
Ammonia can inhibit mitochondrial oxygen consumption and decrease SCFA catabolism by IECs, which has led to the assumption that excess ammonia production can negatively impact the host [ 87 , 88 , 89 ].
However, the gut microbiota also rapidly assimilates ammonia into microbial amino acid biosynthetic processes [ 13 ], and host IECs can additionally control ammonia concentration through conversion to citrulline and glutamine, or through slow release into the bloodstream [ 90 , 91 ].
It is thus unclear how much protein catabolism is necessary to achieve toxic ammonia concentrations, and this may vary between hosts. This uncertainty, coupled with the multiple negative impacts amines can have on the host discussed below , have led to speculation that deamination would improve host outcomes.
Fortunately, deamination appears to be the more common strategy of amino acid catabolism by the gut microbiota, because high concentrations of SCFAs are produced from amino acid degradation via this pathway [ 12 , 13 ].
The next steps depend on the class of amino acid starting substrate, with most eventually resulting in tricarboxylic acid cycle intermediates, pyruvate, or coenzyme A-linked SCFA precursors [ 39 , 75 ]. An exception would be the series of Stickland reactions exhibited by certain Clostridia , in which a coupled oxidation and reduction of two amino acids occurs as an alternative to using hydrogen ions as the electron acceptor [ 40 , 41 ].
Phosphate is simultaneously added to the reduced amino acid in this case, and thus oxidative phosphorylation for the production of ATP can occur directly from the resultant acyl phosphate.
In turn, branched-chain fatty acids BCFAs , such as isovalerate and isobutyrate, can be produced as end-products. Additionally, some gut microbial species, mainly from the class Bacilli, also possess a specialized branched-chain keto acid dehydrogenase complex to yield energy from the oxidized forms of the branched-chain amino acids directly, which also leads to BCFA production [ 13 , 75 ].
The major SCFA and BCFA products generated from degradation of each amino acid are presented in Table 2.
BCFAs are often used as a biomarker of protein catabolism, with the promoted goal to reduce their concentration in order to improve health outcomes [ 14 ].
However, little is actually known about the impact of BCFAs on host health. In fact, preliminary work has shown that BCFAs are able to modulate glucose and lipid metabolism in the liver similarly to SCFAs [ 93 ], and isobutyrate can be used as a fuel source by IECs when butyrate is scarce [ 94 ].
What is undisputed, however, are the negative consequences of the pro-inflammatory, cytotoxic, and neuroactive compounds yielded from the sulfur-containing, basic and aromatic amino acids.
Catabolism of the sulfur-containing amino acids, cysteine and methionine, results in the production of hydrogen sulfide and methanethiol, respectively [ 13 , 14 ], and a large number of taxonomically diverse bacterial species contain the requisite degradative enzymes within their genomes, including members of the Proteobacteria phylum, the Bacilli class, and the Clostridium and Bifidobacterium genera [ 13 , 75 ].
Hydrogen sulfide can be methylated to methanethiol, which can be further methylated to dimethyl sulfide, and this methylation is thought to be part of the detoxification process due to the progressively less toxic nature of these compounds [ 95 ].
However, methanethiol may also be converted to hydrogen sulfide, then oxidized to sulfate, for detoxification; this sulfate can then be utilized by sulfate-reducing bacteria [ 80 , 81 , 95 ].
Indeed, this latter reaction has been observed in cecal tissue, and is part of the sulfur cycle of the gut [ 96 ]. A wide diversity of bacterial species within the gut microbiota can decarboxylate the basic amino acids, thus resulting in the formation of amine by-products shown in Additional file 1 , including bifidobacteria, clostridia , lactobacilli, enterococci, streptococci, and members of the Enterobacteriaceae family [ 97 ].
Agmatine inhibits the proliferation of IECs, which is thought to stem from its ability to reduce the synthesis and promote the degradation of other polyamines [ 98 ]. This effect may not be negative depending on the context; for example, the resultant decrease of fatty acid metabolism in tissues reduced both weight gain and the hormonal derangements associated with obesity in rats fed a high fat chow [ 99 ].
Agmatine also may be anti-inflammatory through inhibition of nitric oxide synthase [ ], and is a candidate neurotransmitter, with agonism for α 2 -adenoceptors and imidazoline binding sites, while simultaneously blocking ligand-gated cation channels NMDA class [ ].
The latter activity has therapeutic potential for remediating some forms of hyperalgesia and for its neuroprotectivity. Putrescine, on the other hand, is essential for the proliferation of IECs [ ]. All three polyamines improve the integrity of the gut by increasing expression of tight junction proteins [ ], promoting intestinal restitution [ ] and increasing mucus secretion [ , ].
Finally, both putrescine and spermine are able to inhibit the production of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α [ , ]. Therefore, any benefits of agmatine must be weighed against its consequent reduction of these polyamines; it may be effective in the treatment of certain conditions such as metabolic syndrome but could be detrimental in excess under normal conditions.
Arginine can additionally be converted to glutamate, which can be deaminated to produce 4-aminobutryate GABA. GABA is the major inhibitory neurotransmitter of the central nervous system, and alterations in the expression of its receptor have been linked to the pathogenesis of depression and anxiety [ ].
Administration of lactobacilli and bifidobacteria that produce GABA to mice and rats has resulted in a decrease of depressive behaviors, a reduction of corticosterone induced stress and anxiety, and lessened visceral pain sensation [ , , ].
GABA can additionally regulate the proliferation of T cells and thus has immunomodulatory properties [ ]. Interestingly, chronic GI inflammation not only induces anxiety in mice, but depression and anxiety often present comorbidity with GI disorders, including irritable bowel syndrome IBS [ , ].
The catabolism of histidine can produce histamine Additional file 1. Histamine may be synonymous with its exertion of inflammation in allergic responses, but bacterially produced histamine has actually been shown to inhibit the production of the pro-inflammatory cytokines TNF-α in vivo [ ], and IL-1, and IL in vitro [ ], while simultaneously preventing intestinal bacterial translocation.
Histamine is also a neurotransmitter, modulating several processes such as wakefulness, motor control, dendritic cell activity, pain perception, and learning and memory [ ]. The catabolism of lysine can produce cadaverine Additional file 1.
Cadaverine is a poorly studied metabolite; it can be toxic, but only in high amounts [ 13 , 97 ]. Cadaverine has, however, been shown to potentiate histamine toxicity [ ] and higher concentrations of cadaverine are associated with ulcerative colitis UC [ ].
Aromatic amino acid degradation can yield a wide diversity of indolic and phenolic compounds that can act as toxins or neurotransmitters as shown in Additional file 2.
The catabolism of tryptophan can produce tryptamine and indoles Additional file 2. Tryptamine is a neurotransmitter that plays a role in regulating intestinal motility and immune function [ ]. Particularly, it is able to interact with both indoleamine 2,3-dioxygenase and the aryl hydrocarbon receptor to heighten immune surveillance, and dampen the expression of pro-inflammatory cytokines, respectively [ , ].
A lack of these activities has therefore been implicated in the pathology of IBD; although, it should be noted that most tryptophan metabolites can interact with these receptors, thus it is not tryptamine-specific [ 13 , , ].
Tryptamine can also both potentiate the inhibitory response of cells to serotonin and induce its release from enteroendocrine cells [ , ]. Serotonin is a neurotransmitter involved in many processes including mood, appetite, hemostasis, immunity, and bone development [ 13 , ].
Its dysregulation is thus reported in many disorders, including IBD [ ], IBS [ ], cardiovascular disease [ ], and osteoporosis [ ]. Tryptophan decarboxylation is a rare activity among species of the gut microbiota, but certain Firmicutes have been found to be capable of it, including the IBD-associated species, Ruminococcus gnavus [ , ].
Indole, on the other hand, is a major bacterial metabolite of tryptophan, produced by many species of Bacteroides and Enterobacteriaceae [ ].
It plays an important role in host defense, by interacting with the pregnane X receptor and the aryl hydrocarbon receptor [ ]. This activity fortifies the intestinal barrier by increasing tight junction protein expression and downregulates the expression of pro-inflammatory cytokines [ , ].
It also induces glucagon like peptide-1 an incretin secretion by enteroendocrine cells, inhibiting gastric secretion and motility, to promote satiety [ , ]. Indole is additionally a signaling molecule for bacteria, influencing motility, biofilm formation, antibiotic resistance, and virulence, and shown to inhibit the colonization capabilities of pathogens such as Salmonella enterica [ ].
However, indole overproduction can increase its export to the liver, where it is sulfated to indoxyl sulfate, a uremic toxin associated with chronic kidney disease [ ].
Further, its effects as a signaling molecule for both enteroendocrine cells and bacteria are dose dependent, with high concentrations rendering it ineffective [ , , ]. The catabolism of tyrosine can produce tyramine, phenols, and p-coumarate Additional file 2.
Tyramine is a neurotransmitter that can be produced by certain gut bacteria via decarboxylation, including Enterococcus and Enterobacteriaceae [ 97 ]. Tyramine facilitates the release of norepinephrine that induces peripheral vasoconstriction, elevates blood glucose levels, and increases cardiac output and respiration [ ].
It has also been shown to increase the synthesis of serotonin by enteroendocrine cells in the gut, elevating its release into circulation [ ]. Phenol and p-cresol are phenolic metabolites that have been shown to both decrease the integrity of the gut epithelium and the viability of IECs [ , ], and can be produced by many gut bacterial species, such as members of the Enterobacteriaceae and Clostridium clusters I, XI, and XIVa [ ].
P-cresol in particular is genotoxic, elevates the production of superoxide, and inhibits proliferation of IECs [ ]. P-cresol may additionally be sulfated to cresyl sulfate in the gut or liver, which has been found to suppress the T helper 1-mediated immune response in mice [ ], and, interestingly, phenolic sulfation was found to be impaired in the gut mucosa of UC patients [ ].
Indeed, the colonic damage induced by unconjugated phenols is similar to that observed in IBD [ ]. Cresyl sulfate is also associated with chronic kidney disease, however, as it can damage renal tubular cells through induction of oxidative stress [ ].
This compound is also particularly elevated in the urine of autistic patients, but a causative link in this case has not been elucidated [ ].
The catabolism of phenylalanine can produce phenylethylamine and trans-cinnamic acid Additional file 2. Unlike tyrosine and tryptophan, little is known about these phenylalanine-derived metabolites.
Through facilitating the release of catecholamine and serotonin, phenylethylamine in turn elevates mood, energy, and attention [ ]. However, it has been reported that ingesting phenylethylamine can induce headache, dizziness, and discomfort in individuals with a reduced ability to convert it to phenylacetate, suggesting excessive amounts have negative consequences [ ].
These metabolic pathways were found to so far specifically occur within species of Clostridium and Peptostreptococcus , respectively [ , ]. The chlorogenic acid phenotype is associated with both autism and schizophrenia, suggesting a role of altered aromatic amino acid metabolism in these disorders [ , , ].
However, further research is still needed, as there remains no mechanistic explanation of these metabolites toward disease development. Further, both trans-cinnamic acid and p-coumaric acid are negatively associated with cardiovascular disease [ , ]. P-coumaric acid, in particular, is a common phenolic compound derived from plant matter that has anti-inflammatory properties, and has been demonstrated to prevent platelet aggregation [ ].
Thus, these metabolites may simply be an indicator of altered microbial metabolism in general, when found in excess. Microorganisms in the gut are known to possess lipases, which can degrade triglycerides and phospholipids into their polar head groups and free lipids [ 16 , ].
Certain bacteria inhabiting the GI tract, including species of lactobacilli, enterococci, clostridia, and Proteobacteria, can utilize the backbone of triglycerides as an electron sink, reducing glycerol to 1,3-propanediol [ ].
Reuterin has antimicrobial properties acting against pathogens and commensals alike [ ], but it can also be spontaneously dehydrated to acrolein [ 71 ].
Acrolein is a highly reactive genotoxin, with an equivalent mutagenic potency to formaldehyde, raising concerns about this metabolic process [ 71 , ].
Meanwhile, choline can additionally be metabolized to trimethylamine by species of the gut microbiota, particularly Clostridia especially members of Clostridium cluster XIVa and Eubacterium spp.
and Proteobacteria [ , ]. Trimethylamine is oxidized in the liver to trimethylamine N-oxide [ , ], which exacerbates atherosclerosis by promoting the formation of foam cells lipid-laden macrophages [ ] and altering cholesterol transport [ ]. High levels of serum trimethylamine N-oxide are thus associated with cardiovascular disease [ ] and atherosclerosis [ ].
However, it should be noted that active research in these areas is in its early stages, and thus the link between the gut microbiota-mediated lipid head group metabolism and health consequences is still unclear.
For example, a study on the metabolism of glycerol by fecal microbial communities found that only a subset could reduce it to 1,3-propanediol, and the authors did not detect any reuterin [ ]. Further, some members of the gut microbiota e.
In contrast to the polar head groups, microorganisms are not thought to have the ability to catabolize free lipids in the anaerobic environment of the gut [ ]. However, free lipids have antimicrobial properties [ , ] and can directly interact with host pattern recognition receptors.
Particularly, saturated fatty acids are TLR4 agonists that promote inflammation [ ], whereas omega-3 unsaturated fatty acids are TLR4 antagonists that prevent inflammation [ ]. Interestingly, chronic inflammation co-occurring with obesity has been well described [ ], and could be a result of the aforementioned pro-inflammatory properties of free lipids, the lack of anti-inflammatory SCFAs produced from carbohydrate fermentation high-fat diets tend to be low in carbohydrates , or a combination of both.
High-fat diets do have a reported impact on the composition of the gut microbiota, yet it is unclear whether it is the increased fat content per se or the relative decrease in carbohydrates, which often accompanies these diets, that is the chief influencer [ 16 , ].
Indeed, Morales et al. observed that a high-fat diet including fiber supplementation induces inflammation without altering the composition of the gut microbiota [ 16 ]. Regardless, the gut microbiota is required for the development of obesity, as shown in GF mice experiments, because of the ability of SCFAs to alter energy balance as previously discussed [ ].
Metabolism of exogenous substrates greatly affects the use of endogenous substrates by the gut microbiota. Dietary fiber reduces the degradation of mucin, and the utilization of mucin is thought to cycle daily depending on the availability of food sources [ , ].
Mucin is a sulfated glycoprotein [ 38 ], thus the same concepts of carbohydrate and protein degradation from dietary sources discussed above apply. However, it should be noted that mucin turnover by the gut microbiota is a naturally occurring process, and only when it occurs in elevated amounts does it have negative connotations.
For example, Akkermansia muciniphila is a mucin-utilizing specialist that is depleted in the GI tract of IBD [ ] and metabolic syndrome [ ] patients. muciniphila has a demonstrated ability to cross-talk with host cells, promoting an increase in concentration of glucagon-like peptides, 2-arabinoglycerol, and antimicrobial peptides that improve barrier function, reduce inflammation, and induce proliferation of IECs [ ].
Through this communication, A. muciniphila also, paradoxically, restored the thickness of the mucin layer in obese mice. Dietary fat intake can also alter the profile of bile acids. Dairy-derived saturated lipids increase the relative amount of taurine-conjugation, and this sulfur-containing compound leads to the expansion of sulfate-reducing bacteria in the gut [ ].
Bile acid turnover is, however, a naturally occurring process, which modulates bile acid reabsorption, inflammation, triglyceride control, and glucose homeostasis from IEC signaling [ ]. The critical contributions of the gut microbiota toward human digestion have just begun to be elucidated.
Particularly, more recent research is revealing how the impacts of microbial metabolism extend beyond the GI tract, denoting the so-called gut-brain e. The primary focus to date has been on the SCFAs derived mainly from complex carbohydrates, and crucial knowledge gaps still remain in this area, specifically on how the SCFAs modulate glucose metabolism and fat deposition upon reaching the liver.
However, the degradation of proteins and fats are comparatively less well understood. Due to both the diversity of metabolites that can be yielded and the complexity of microbial pathways, which can act as a self-regulating system that removes toxic by-products, it is not merely a matter of such processes effecting health positively or negatively, but rather how they are balanced.
Further, the presentation of these substrates to the gut microbiota, as influenced by the relatively understudied host digestive processes occurring in the small intestine, is equally important. Future work could therefore aim to determine which of these pathways are upregulated and downregulated in disease states, such as autism and depression gut-brain , NAFLD gut-liver , chronic kidney disease gut-kidney , and cardiovascular disease gut-heart.
Further, a combination of human- and culture- in vitro and in vivo based studies could resolve the spectrum of protein and fat degradation present among healthy individuals, in order to further our understanding of nutrient cycling in gut microbial ecosystems, and thus gain a necessary perspective for improving wellness.
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In addition, one study suggests that bacterial fermentation of fiber increased GLP-1 by increasing the number of GLP-1 secreting L-cells. The effect can also go the other way: Some bacteria impair GLP-1 receptors, leading to GLP-1 resistance. Bile acids are another example. Produced by the liver and released into the small intestine, they are processed by gut bacteria, and can also stimulate GLP-1 secretion from the L-cells.
So changes in the gut microbiome that reduce SCFA-producing bacteria or bile acid-processing bacteria may have consequences in GLP-1 signaling, which can impact our ability to process glucose efficiently. Chronic inflammation underlies many metabolic disorders.
One pathway to that inflammation is when elements in the gut leak through the gut lining and enter our system—a condition termed metabolic endotoxemia.
What prevents that leaking is the so-called gut barrier , a multi-layer physical and functional system separating the gut from the rest of the body. The gut barrier is lined with a single, intact layer of epithelial cells similar to cells that cover the surface of the body, such as the skin that absorbs nutrients and protects from invading pathogens.
A layer of mucus covers the inside of that gut epithelium; on the other side are immune cells tasked with surveillance against microbes that may attempt to escape from the gut and enter the body. Studies in animal models show that the microbiome regulates different components of this gut barrier defense mechanism.
The mucus is created by specialized goblet cells in the gut lining to coat and protect the epithelial cells from microbes and digestive enzymes. This viscous layer is also infused with a diverse array of antimicrobial agents and antibodies as additional protection.
Without a gut microbiome, germ-free mice have a thinner mucosal layer and fewer antimicrobial agents—traits often associated with metabolic and immunological diseases.
Similarly, a fiber-deprived diet shifts the gut microbiome to consume rather than build up the mucus, resulting in a compromised gut barrier. On the other hand, probiotic supplementation and fiber-rich dietary interventions can restore a healthy mucus barrier.
Covered and protected by the mucosa is the selectively permeable barrier made of epithelial cells. The cells are bound together by specialized tight junction proteins that allow only desired nutrients to pass through.
In many inflammatory diseases , these tight junction proteins are reduced or not functional, allowing harmful microbes and toxins to enter. The gut microbiome also influences tight junctions , which can, at least in animals, be restored by probiotics and dietary fiber.
A blood biomarker, Lipopolysaccharide LPS , allows us to measure a dysfunctional gut barrier. Probiotics , dietary fiber , and other nutritional interventions have been shown to lower the level of blood LPS, as well as markers of inflammation, in people with obesity and diabetes. Inflammation helps heal your body, but chronic inflammation can cause serious damage.
Beyond the gut barrier, the gut microbiome can also shape the immune system to be more resilient to fight invaders while being less damaging to the body. Inflammation is a double-edged sword: it protects the body from infection and injury, but excessive inflammation can be damaging.
Therefore a balance, or immune homeostasis , is crucial. Unfortunately, the modern lifestyle puts the body under constant stress, and the result is a chronic low-grade inflammation that underlies many diseases.
The gut is home to the largest number of immune cells within the body, and the gut microbiome and its metabolites are known drivers of the immune repertoire. In addition to the antimicrobial function at the mucosal barrier, normal gut bacteria help develop immune cells that fight pathogenic microbes.
Other bacteria directly increase regulatory T cells , an important immune cell type that suppresses inflammation and keeps the body from attacking itself. Again, microbially produced SCFA are important players behind this mechanism , along with vitamin A-derived retinoic acids.
On the flip side, dietary and probiotic-mediated gut microbiome changes have been shown to blunt inflammation, presenting possible microbiome-based solutions for inflammatory diseases. Diet shapes the gut microbiome. The modern Western diet is low on fiber and high in unnatural additives—this combination reduces or removes certain groups of microbes from the gut.
When those conditions persist, the weakened gut microbiome damages our immune and metabolic functions in the ways shown above, which further harms the microbiome, creating a negative feedback loop.
While we need more controlled human-intervention studies, research thus far suggests that some simple interventions can reduce damages in microbiome-regulated metabolic and immune functions.
The benefits of fiber-rich food are well known— fiber slows your digestion so you stay fuller longer, and it promotes blood-sugar and cholesterol control. We have seen above that the gut microbiome has everything to do with these benefits. Fiber-rich foods— such as beans , legumes, fresh vegetables , nuts , seeds, fruit , and whole grains —are particularly good at supporting the growth of beneficial gut microbes that regulate metabolic hormones and reduce inflammation.
In addition, polyphenol-rich foods, including green tea and berries, appear to modulate the gut microbiome and increase beneficial groups of bacteria. Prebiotic supplements pack specific types of fiber known to feed selective groups of bacteria that confer health benefits.
Taking prebiotic supplements is an excellent way to ensure you foster the growth of these bacteria. Inulin, which occurs naturally in high concentrations in chicory root and Jerusalem artichokes, is a fiber source that supports the desirable microbes and is available in multiple prebiotic supplements.
If your gut microbiome has already suffered from a prolonged Western diet, just adding back fiber in the short-term will not be enough to completely restore beneficial bacteria.
While both may be beneficial, it is important to understand that you can maximize the benefit by understanding the needs of your very unique gut microbiome. These needs have been identified in studies that have profiled the microbiome changes associated with various diseases, and may sometimes be echoed in personal microbiome testing results.
Pendulum Therapeutics, Inc. has authored this review article, with editorial assistance from Levels.
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