Gut microbiota

<h2 id="overview">Overview</h2>

In humans, the gut microbiota has the highest numbers and species of bacteria compared to other areas of the body.<a class="footnote-ref" id="fnref:11" href="#fn:11">11</a> The approximate number of bacteria composing the gut microbiota is about 1013–1014 (10,000 to 100,000 billion).<a class="footnote-ref" id="fnref:12" href="#fn:12">12</a> In humans, the gut flora is established at birth and gradually transitions towards a state resembling that of adults by the age of two,<a class="footnote-ref" id="fnref:13" href="#fn:13">13</a> coinciding with the development and maturation of the <a href="/facts/Intestinal_epithelium/32hWmspE">intestinal epithelium</a> and <a href="/facts/Intestinal_mucosal_barrier/2xRUUfrd">intestinal mucosal barrier</a>. This barrier is essential for supporting a symbiotic relationship with the gut flora while providing protection against pathogenic organisms.<a class="footnote-ref" id="fnref:14" href="#fn:14">14</a><a class="footnote-ref" id="fnref:15" href="#fn:15">15</a>
The relationship between some gut microbiota and humans is not merely <a href="/facts/Commensalism/KnJkboX0">commensal</a> (a non-harmful coexistence), but rather a <a href="/facts/Mutualism_(biology)/29hCDDS2">mutualistic</a> relationship.<a class="footnote-ref" id="fnref:16" href="#fn:16">16</a>: 700  Some human gut microorganisms benefit the host by <a href="/facts/Fermentation/rxaDr28b">fermenting</a> <a href="/facts/Dietary_fiber/Q9DXanDv">dietary fiber</a> into <a href="/facts/Short-chain_fatty_acid/bgj2XGRf">short-chain fatty acids</a> (SCFAs), such as <a href="/facts/Acetic_acid/uyBKA2Pd">acetic acid</a> and <a href="/facts/Butyric_acid/Sy5NrhK5">butyric acid</a>, which are then absorbed by the host.<a class="footnote-ref" id="fnref:17" href="#fn:17">17</a><a class="footnote-ref" id="fnref:18" href="#fn:18">18</a> Intestinal <a href="/facts/Bacteria/wC8xSCsU">bacteria</a> also play a role in synthesizing certain <a href="/facts/B_vitamins/m6ekXy6A">B vitamins</a> and <a href="/facts/Vitamin_K/dpTFSa4J">vitamin K</a> as well as metabolizing <a href="/facts/Bile_acid/ojTJzf0c">bile acids</a>, <a href="/facts/Sterol/QrVlPnWn">sterols</a>, and <a href="/facts/Xenobiotic/0M2LAyEx">xenobiotics</a>.<a class="footnote-ref" id="fnref:19" href="#fn:19">19</a><a class="footnote-ref" id="fnref:20" href="#fn:20">20</a> The systemic importance of the SCFAs and other compounds they produce are like <a href="/facts/Hormones/WFnBnINJ">hormones</a> and the gut flora itself appears to function like an <a href="/facts/Gland/gfq2of7k">endocrine organ</a>.<a class="footnote-ref" id="fnref:21" href="#fn:21">21</a> Dysregulation of the gut flora has been correlated with a host of inflammatory and autoimmune conditions.<a class="footnote-ref" id="fnref:22" href="#fn:22">22</a><a class="footnote-ref" id="fnref:23" href="#fn:23">23</a>
The composition of human gut microbiota changes over time, when the diet changes, and as overall health changes.<a class="footnote-ref" id="fnref:24" href="#fn:24">24</a><a class="footnote-ref" id="fnref:25" href="#fn:25">25</a> A <a href="/facts/Systematic_review/dGvq3BGx">systematic review</a> from 2016 examined the preclinical and small human trials that have been conducted with certain commercially available strains of probiotic bacteria and identified those that had the most potential to be useful for certain <a href="/facts/Central_nervous_system_disorder/EGlB2D4w">central nervous system disorders</a>.<a class="footnote-ref" id="fnref:26" href="#fn:26">26</a> It should also be highlighted that the Mediterranean diet, rich in vegetables and fibers, stimulates the activity and growth of beneficial bacteria for the brain.<a class="footnote-ref" id="fnref:27" href="#fn:27">27</a>

<h2 id="classifications">Classifications</h2>
The microbial composition of the gut microbiota varies across the digestive tract. In the <a href="/facts/Stomach/Q4PPDGT6">stomach</a> and <a href="/facts/Small_intestine/1AQ8RJ4m">small intestine</a>, relatively few species of bacteria are generally present.<a class="footnote-ref" id="fnref:28" href="#fn:28">28</a><a class="footnote-ref" id="fnref:29" href="#fn:29">29</a> <a href="/facts/Fungi/BHo5DP59">Fungi</a>, <a href="/facts/Protist/NYVfaGVz">protists</a>, <a href="/facts/Archaea/Adxh0aHw">archaea</a>, and <a href="/facts/Virus/mf88Bcbl">viruses</a> are also present in the gut flora, but less is known about their activities.<a class="footnote-ref" id="fnref:30" href="#fn:30">30</a>

Many species in the gut have not been studied outside of their hosts because they cannot be <a href="/facts/Microbiological_culture/y3VaXn9Q">cultured</a>.<a class="footnote-ref" id="fnref:31" href="#fn:31">31</a><a class="footnote-ref" id="fnref:32" href="#fn:32">32</a><a class="footnote-ref" id="fnref:33" href="#fn:33">33</a> While there are a small number of core microbial species shared by most individuals, populations of microbes can vary widely.<a class="footnote-ref" id="fnref:34" href="#fn:34">34</a> Within an individual, their microbial populations stay fairly constant over time, with some alterations occurring due to changes in lifestyle, diet and age.<a class="footnote-ref" id="fnref:35" href="#fn:35">35</a><a class="footnote-ref" id="fnref:36" href="#fn:36">36</a> The <a href="/facts/Human_Microbiome_Project/yqBkY8PL">Human Microbiome Project</a> has set out to better describe the <a href="/facts/Microbiota/V4ymrawz">microbiota</a> of the human gut and other body locations.
The four dominant <a href="/facts/Bacterial_phyla/ChzCDhYl">bacterial phyla</a> in the human gut are <a href="/facts/Bacillota/FxP0p0n8">Bacillota</a> (Firmicutes), <a href="/facts/Bacteroidota/D8vX8BHh">Bacteroidota</a>, <a href="/facts/Actinomycetota/ShmuHEND">Actinomycetota</a>, and <a href="/facts/Pseudomonadota/ggjeK6II">Pseudomonadota</a>.<a class="footnote-ref" id="fnref:37" href="#fn:37">37</a> Most bacteria belong to the genera <a href="/facts/Bacteroides/Ln9hkTdc">Bacteroides</a>, <a href="/facts/Clostridium/HRXJyYCn">Clostridium</a>, <a href="/facts/Faecalibacterium/pyweMtzx">Faecalibacterium</a>,<a class="footnote-ref" id="fnref:38" href="#fn:38">38</a><a class="footnote-ref" id="fnref:39" href="#fn:39">39</a> <a href="/facts/Eubacterium/I9QLVuj1">Eubacterium</a>, <a href="/facts/Ruminococcus/bl6a6t0p">Ruminococcus</a>, <a href="/facts/Peptococcus/7p0LBxRF">Peptococcus</a>, <a href="/facts/Peptostreptococcus/R0r7yIC4">Peptostreptococcus</a>, and <a href="/facts/Bifidobacterium/ov3Sghxb">Bifidobacterium</a>.<a class="footnote-ref" id="fnref:40" href="#fn:40">40</a><a class="footnote-ref" id="fnref:41" href="#fn:41">41</a> Other genera, such as <a href="/facts/Escherichia/ehBXfPgT">Escherichia</a> and <a href="/facts/Lactobacillus/pwoacAbe">Lactobacillus</a>, are present to a lesser extent.<a class="footnote-ref" id="fnref:42" href="#fn:42">42</a> Species from the genus Bacteroides alone constitute about 30% of all bacteria in the gut, suggesting that this genus is especially important in the functioning of the host.<a class="footnote-ref" id="fnref:43" href="#fn:43">43</a>
Fungal genera that have been detected in the gut include <a href="/facts/Candida_(genus)/IIYvWvx5">Candida</a>, <a href="/facts/Saccharomyces/uvqNvGje">Saccharomyces</a>, <a href="/facts/Aspergillus/pKhecLTW">Aspergillus</a>, <a href="/facts/Penicillium/6mFbS6zl">Penicillium</a>, <a href="/facts/Rhodotorula/4g2ls4pI">Rhodotorula</a>, <a href="/facts/Trametes/hU04XWdY">Trametes</a>, <a href="/facts/Pleospora/6kWYvJaP">Pleospora</a>, <a href="/facts/Sclerotinia/edUptxuf">Sclerotinia</a>, <a href="/facts/Bullera/KSNLa70b">Bullera</a>, and <a href="/facts/Galactomyces/SJgcIw0o">Galactomyces</a>, among others.<a class="footnote-ref" id="fnref:44" href="#fn:44">44</a><a class="footnote-ref" id="fnref:45" href="#fn:45">45</a> Rhodotorula is most frequently found in individuals with <a href="/facts/Inflammatory_bowel_disease/RuxcPW5A">inflammatory bowel disease</a> while Candida is most frequently found in individuals with hepatitis B cirrhosis and chronic hepatitis B.<a class="footnote-ref" id="fnref:46" href="#fn:46">46</a>
<a href="/facts/Methanobrevibacter_smithii/GK0TTAQJ">Archaea</a> constitute another large class of gut flora which are important in the metabolism of the bacterial products of fermentation.
<a href="/facts/Industrialisation/h3QXzS6C">Industrialization</a> is associated with changes in the microbiota and the reduction of diversity could drive certain species to extinction; in 2018, researchers proposed a <a href="/facts/Biobank/cQEQqdcl">biobank</a> repository of human microbiota.<a class="footnote-ref" id="fnref:47" href="#fn:47">47</a>

<h3>Enterotype</h3>
An <a href="/facts/Enterotype/L622z7F5">enterotype</a> is a classification of living organisms based on its bacteriological <a href="/facts/Ecosystem/kVE8mSmR">ecosystem</a> in the human gut microbiome not dictated by age, gender, body weight, or national divisions.<a class="footnote-ref" id="fnref:48" href="#fn:48">48</a> There are indications that long-term diet influences enterotype.<a class="footnote-ref" id="fnref:49" href="#fn:49">49</a> Three human enterotypes have been proposed,<a class="footnote-ref" id="fnref:50" href="#fn:50">50</a><a class="footnote-ref" id="fnref:51" href="#fn:51">51</a> but their value has been questioned.<a class="footnote-ref" id="fnref:52" href="#fn:52">52</a>

<h2 id="composition">Composition</h2>
See also: <a href="/facts/Human_microbiome/xJIRMUAY">Human microbiome § Gastrointestinal tract</a>

<h3>Bacteria</h3>
<h4>Stomach</h4>
Due to the high acidity of the <a href="/facts/Stomach/Q4PPDGT6">stomach</a>, most microorganisms cannot survive there. The main bacteria of the gastric microbiota belong to five major phyla: <a href="/facts/Firmicutes/Ic9CrSe7">Firmicutes</a>, <a href="/facts/Bacteroidetes/EA9L6clb">Bacteroidetes</a>, <a href="/facts/Actinobacteria_(class)/vBImrRr7">Actinobacteria</a>, <a href="/facts/Fusobacteriota/JhCYSFjp">Fusobacteriota</a>, and <a href="/facts/Proteobacteria/m7SfxPus">Proteobacteria</a>. The dominant genera are <a href="/facts/Prevotella/9v28vwna">Prevotella</a>, <a href="/facts/Streptococcus/Fx8lJ0nz">Streptococcus</a>, <a href="/facts/Veillonella/4oaT892T">Veillonella</a>, <a href="/facts/Rothia_(bacterium)/LcD2mbwy">Rothia</a>, and <a href="/facts/Haemophilus/uKcnj55j">Haemophilus</a>.<a class="footnote-ref" id="fnref:53" href="#fn:53">53</a> The interaction between the pre-existing gastric microbiota with the introduction of <a href="/facts/H._pylori/9q4H68LP">H. pylori</a> may influence <a href="/facts/Helicobacter_pylori/9q4H68LP">disease progression</a>.<a class="footnote-ref" id="fnref:54" href="#fn:54">54</a> When there is a presence of H. pylori it becomes the dominant species of the microbiota.<a class="footnote-ref" id="fnref:55" href="#fn:55">55</a>

<h4>Intestines</h4>
<table><tbody><tr><td colspan="2">Bacteria commonly found in the human colon<a class="footnote-ref" id="fnref:56" href="#fn:56">56</a></td></tr><tr><th>Bacterium</th><th>Incidence (%)</th></tr><tr><td><a href="/facts/Bacteroides_fragilis/94ovcupK">Bacteroides fragilis</a></td><td>100</td></tr><tr><td><a href="/facts/Bacteroides_melaninogenicus/X05BtcAz">Bacteroides melaninogenicus</a></td><td>100</td></tr><tr><td>Bacteroides oralis</td><td>100</td></tr><tr><td><a href="/facts/Enterococcus_faecalis/66cjKlxr">Enterococcus faecalis</a></td><td>100</td></tr><tr><td><a href="/facts/Escherichia_coli/nR4Gvl56">Escherichia coli</a></td><td>100</td></tr><tr><td><a href="/facts/Enterobacter/MErC2JkH">Enterobacter</a> sp.</td><td>40–80</td></tr><tr><td><a href="/facts/Klebsiella/mRzCFEfA">Klebsiella</a> sp.</td><td>40–80</td></tr><tr><td><a href="/facts/Bifidobacterium_bifidum/HPcXF7U3">Bifidobacterium bifidum</a></td><td>30–70</td></tr><tr><td><a href="/facts/Staphylococcus_aureus/9yDVBMsc">Staphylococcus aureus</a></td><td>30–50</td></tr><tr><td><a href="/facts/Lactobacillus/pwoacAbe">Lactobacillus</a></td><td>20–60</td></tr><tr><td><a href="/facts/Clostridium_perfringens/hhfqd8Sm">Clostridium perfringens</a></td><td>25–35</td></tr><tr><td><a href="/facts/Proteus_mirabilis/awwMoQdt">Proteus mirabilis</a></td><td>5–55</td></tr><tr><td><a href="/facts/Clostridium_tetani/RzFNBHds">Clostridium tetani</a></td><td>1–35</td></tr><tr><td><a href="/facts/Clostridium_septicum/QH4uYc0k">Clostridium septicum</a></td><td>5–25</td></tr><tr><td><a href="/facts/Pseudomonas_aeruginosa/HBhyIxAn">Pseudomonas aeruginosa</a></td><td>3–11</td></tr><tr><td><a href="/facts/Salmonella_enterica/uPm6xd3P">Salmonella enterica</a></td><td>3–7</td></tr><tr><td><a href="/facts/Faecalibacterium_prausnitzii/pyweMtzx">Faecalibacterium prausnitzii</a></td><td>?common</td></tr><tr><td><a href="/facts/Peptostreptococcus/R0r7yIC4">Peptostreptococcus</a> sp.</td><td>?common</td></tr><tr><td><a href="/facts/Peptococcus/7p0LBxRF">Peptococcus</a> sp.</td><td>?common</td></tr></tbody></table>
The small intestine contains a trace amount of microorganisms due to the proximity and influence of the stomach. <a href="/facts/Gram-positive_bacteria/H6WYQ17e">Gram-positive</a> <a href="/facts/Coccus/51QVlEDC">cocci</a> and <a href="/facts/Bacillus_(shape)/0rGR5vvU">rod-shaped bacteria</a> are the predominant microorganisms found in the small intestine.<a class="footnote-ref" id="fnref:57" href="#fn:57">57</a> However, in the distal portion of the small intestine alkaline conditions support gram-negative bacteria of the Enterobacteriaceae.<a class="footnote-ref" id="fnref:58" href="#fn:58">58</a> The bacterial flora of the small intestine aid in a wide range of intestinal functions. The bacterial flora provide regulatory signals that enable the development and utility of the gut. Overgrowth of bacteria in the small intestine can lead to intestinal failure.<a class="footnote-ref" id="fnref:59" href="#fn:59">59</a> In addition the large intestine contains the largest bacterial ecosystem in the human body.<a class="footnote-ref" id="fnref:60" href="#fn:60">60</a> About 99% of the large intestine and feces flora are made up of obligate anaerobes such as Bacteroides and Bifidobacterium.<a class="footnote-ref" id="fnref:61" href="#fn:61">61</a> Factors that disrupt the microorganism population of the large intestine include antibiotics, stress, and parasites.<a class="footnote-ref" id="fnref:62" href="#fn:62">62</a>
Bacteria make up most of the flora in the <a href="/facts/Colon_(anatomy)/vQtlNBv9">colon</a><a class="footnote-ref" id="fnref:63" href="#fn:63">63</a> and accounts for 60% of <a href="/facts/Fecal/r9HDKB8G">fecal</a> nitrogen.<a class="footnote-ref" id="fnref:64" href="#fn:64">64</a> This fact makes feces an ideal source of gut flora for any tests and experiments by extracting the nucleic acid from fecal specimens, and bacterial 16S rRNA gene sequences are generated with bacterial primers. This form of testing is also often preferable to more invasive techniques, such as biopsies.
Five <a href="/facts/Phylum/ELT3Jyax">phyla</a> dominate the intestinal microbiota: <a href="/facts/Bacteroidota/D8vX8BHh">Bacteroidota</a>, <a href="/facts/Bacillota/FxP0p0n8">Bacillota</a> (Firmicutes), <a href="/facts/Actinomycetota/ShmuHEND">Actinomycetota</a>, <a href="/facts/Pseudomonadota/ggjeK6II">Pseudomonadota</a>, and <a href="/facts/Verrucomicrobiota/mvsaIoJ0">Verrucomicrobiota</a> – with Bacteroidota and Bacillota constituting 90% of the composition.<a class="footnote-ref" id="fnref:65" href="#fn:65">65</a> Somewhere between 300<a class="footnote-ref" id="fnref:66" href="#fn:66">66</a> and 1000 different <a href="/facts/Species/oDg6b96r">species</a> live in the gut,<a class="footnote-ref" id="fnref:67" href="#fn:67">67</a> with most estimates at about 500.<a class="footnote-ref" id="fnref:68" href="#fn:68">68</a><a class="footnote-ref" id="fnref:69" href="#fn:69">69</a> However, it is probable that 99% of the bacteria come from about 30 or 40 species, with <a href="/facts/Faecalibacterium_prausnitzii/pyweMtzx">Faecalibacterium prausnitzii</a> (phylum firmicutes) being the most common species in healthy adults.<a class="footnote-ref" id="fnref:70" href="#fn:70">70</a><a class="footnote-ref" id="fnref:71" href="#fn:71">71</a>
Research suggests that the relationship between gut <a href="/facts/Flora_(microbiology)/YnAvJQvV">flora</a> and humans is not merely <a href="/facts/Commensalism/KnJkboX0">commensal</a> (a non-harmful coexistence), but rather is a <a href="/facts/Mutualism_(biology)/29hCDDS2">mutualistic</a>, <a href="/facts/Symbiosis/MrBArRGa">symbiotic</a> relationship.<a class="footnote-ref" id="fnref:72" href="#fn:72">72</a> Though people can survive with no gut flora,<a class="footnote-ref" id="fnref:73" href="#fn:73">73</a> the microorganisms perform a host of useful functions, such as <a href="/facts/Fermentation_(biochemistry)/rxaDr28b">fermenting</a> unused energy substrates, training the <a href="/facts/Immune_system/HRCTf1pb">immune system</a> via end products of metabolism like <a href="/facts/Propionate/ugBEw0Ia">propionate</a> and <a href="/facts/Acetate/U90VVczy">acetate</a>, preventing growth of harmful species, regulating the development of the gut, producing vitamins for the host (such as <a href="/facts/Biotin/WAaVxyB7">biotin</a> and <a href="/facts/Vitamin_K/dpTFSa4J">vitamin K</a>), and producing hormones to direct the host to store fats.<a class="footnote-ref" id="fnref:74" href="#fn:74">74</a> Extensive modification and imbalances of the gut microbiota and its microbiome or gene collection are associated with obesity.<a class="footnote-ref" id="fnref:75" href="#fn:75">75</a> However, in certain conditions, some species are thought to be capable of causing <a href="/facts/Disease/55eeQlGL">disease</a> by causing <a href="/facts/Infection/182XrncP">infection</a> or increasing <a href="/facts/Cancer/PVW6n1D0">cancer</a> risk for the host.<a class="footnote-ref" id="fnref:76" href="#fn:76">76</a><a class="footnote-ref" id="fnref:77" href="#fn:77">77</a>

<h3>Fungi</h3>
Further information: <a href="/facts/Mycobiome/yhajkIoc">Mycobiome</a>
<a href="/facts/Fungus/BHo5DP59">Fungi</a> also make up a part of the gut flora, but less is known about their activities.<a class="footnote-ref" id="fnref:78" href="#fn:78">78</a>
Due to the prevalence of fungi in the natural environment, determining which genera and species are permanent members of the gut <a href="/facts/Mycobiome/yhajkIoc">mycobiome</a> is difficult.<a class="footnote-ref" id="fnref:79" href="#fn:79">79</a><a class="footnote-ref" id="fnref:80" href="#fn:80">80</a> Research is underway as to whether Penicillium is a permanent or transient member of the gut flora, obtained from dietary sources such as <a href="/facts/Cheese/JrG8nGCm">cheese</a>, though several species in the genus are known to survive at temperatures around 37 °C, about the same as the <a href="/facts/Human_body_temperature/zbWKsEhF">core body temperature</a>.<a class="footnote-ref" id="fnref:81" href="#fn:81">81</a> <a href="/facts/Saccharomyces_cerevisiae/sX9MGFrz">Saccharomyces cerevisiae</a>, brewer's yeast, is known to reach the intestines after being ingested and can be responsible for the condition <a href="/facts/Auto-brewery_syndrome/CwXXNxP2">auto-brewery syndrome</a> in cases where it is overabundant,<a class="footnote-ref" id="fnref:82" href="#fn:82">82</a><a class="footnote-ref" id="fnref:83" href="#fn:83">83</a><a class="footnote-ref" id="fnref:84" href="#fn:84">84</a> while <a href="/facts/Candida_albicans/7o27aEFS">Candida albicans</a> is likely a permanent member, and is believed to be acquired at birth through <a href="/facts/Vertical_transmission/5KmmumIw">vertical transmission</a>.<a class="footnote-ref" id="fnref:85" href="#fn:85">85</a>[medical citation needed]

<h3>Viruses</h3>
Further information: <a href="/facts/Virome/4ekjsjnk">Virome</a>
The <a href="/facts/Human_virome/VwyIjjS3">human virome</a> includes all viruses associated with the human body, ranging from viruses that infect native cells to bacteriophages that infect bacteria in the microbiome. Among these, <a href="/facts/Bacteriophage/L2Ll0T3q">bacteriophages</a> are by far the most numerous.<a class="footnote-ref" id="fnref:86" href="#fn:86">86</a>

<h2 id="variation">Variation</h2>
<h3>Age</h3>
There are common patterns of microbiome composition evolution during life.<a class="footnote-ref" id="fnref:87" href="#fn:87">87</a> In general, the diversity of microbiota composition of fecal samples is significantly higher in adults than in children, although interpersonal differences are higher in children than in adults.<a class="footnote-ref" id="fnref:88" href="#fn:88">88</a> Much of the maturation of microbiota into an adult-like configuration happens during the first three years of life.<a class="footnote-ref" id="fnref:89" href="#fn:89">89</a>
As the microbiome composition changes, so does the composition of bacterial proteins produced in the gut. In adult microbiomes, a high prevalence of enzymes involved in <a href="/facts/Fermentation/rxaDr28b">fermentation</a>, <a href="/facts/Methanogenesis/5sA0no5A">methanogenesis</a> and the metabolism of <a href="/facts/Arginine/y49Hdf1e">arginine</a>, <a href="/facts/Glutamate/7oXbNcvu">glutamate</a>, <a href="/facts/Aspartate/9DFSFPa1">aspartate</a> and <a href="/facts/Lysine/CEetgA9L">lysine</a> have been found. In contrast, in infant microbiomes the dominant enzymes are involved in <a href="/facts/Cysteine/kbqvUm6d">cysteine</a> metabolism and fermentation pathways.<a class="footnote-ref" id="fnref:90" href="#fn:90">90</a>

<h3>Geography</h3>
Gut microbiome composition depends on the geographic origin of populations. Variations in a trade-off of <a href="/facts/Prevotella/9v28vwna">Prevotella</a>, the representation of the <a href="/facts/Urease/qh6XKw4w">urease</a> gene, and the representation of genes encoding glutamate synthase/degradation or other enzymes involved in amino acids degradation or vitamin biosynthesis show significant differences between populations from the US, <a href="/facts/Malawi/HTj5q7Wc">Malawi</a>, or Amerindian origin.<a class="footnote-ref" id="fnref:91" href="#fn:91">91</a>
The US population has a high representation of enzymes encoding the degradation of <a href="/facts/Glutamine/t94zX4SK">glutamine</a> and enzymes involved in vitamin and <a href="/facts/Lipoic_acid/9wTHHWBf">lipoic acid</a> biosynthesis; whereas Malawi and Amerindian populations have a high representation of enzymes encoding glutamate synthase and they also have an overrepresentation of <a href="/facts/%25CE%2591-amylase/6xXvngle">α-amylase</a> in their microbiomes. As the US population has a diet richer in fats than Amerindian or Malawian populations which have a corn-rich diet, the diet is probably the main determinant of the gut bacterial composition.<a class="footnote-ref" id="fnref:92" href="#fn:92">92</a>
Further studies have indicated a large difference in the composition of microbiota between European and rural African children. The fecal bacteria of children from <a href="/facts/Florence/Mx0uhNma">Florence</a> were compared to that of children from the small rural village of <a href="/facts/Boulpon/jA9va9FJ">Boulpon</a> in <a href="/facts/Burkina_Faso/L3zPAJwx">Burkina Faso</a>. The diet of a typical child living in this village is largely lacking in fats and animal proteins and rich in polysaccharides and plant proteins. The fecal bacteria of European children were dominated by Firmicutes and showed a marked reduction in biodiversity, while the fecal bacteria of the Boulpon children was dominated by Bacteroidetes. The increased biodiversity and different composition of the gut microbiome in African populations may aid in the digestion of normally indigestible plant polysaccharides and also may result in a reduced incidence of non-infectious colonic diseases.<a class="footnote-ref" id="fnref:93" href="#fn:93">93</a>
On a smaller scale, it has been shown that sharing numerous common environmental exposures in a family is a strong determinant of individual microbiome composition. This effect has no genetic influence and it is consistently observed in culturally different populations.<a class="footnote-ref" id="fnref:94" href="#fn:94">94</a>

<h4>Malnourishment</h4>
<a href="/facts/Malnutrition/KasQy5MR">Malnourished</a> children have less mature and less diverse gut microbiota than healthy children, and changes in the microbiome associated with nutrient scarcity can in turn be a pathophysiological cause of malnutrition.<a class="footnote-ref" id="fnref:95" href="#fn:95">95</a><a class="footnote-ref" id="fnref:96" href="#fn:96">96</a> Malnourished children also typically have more potentially pathogenic gut flora, and more <a href="/facts/Yeast/eGD24nfI">yeast</a> in their mouths and throats.<a class="footnote-ref" id="fnref:97" href="#fn:97">97</a> Altering diet may lead to changes in gut microbiota composition and diversity.<a class="footnote-ref" id="fnref:98" href="#fn:98">98</a>

<h3>Race and ethnicity</h3>
Researchers with the American Gut Project and Human Microbiome Project found that twelve microbe families varied in abundance based on the race or ethnicity of the individual. The strength of these associations is limited by the small sample size: the American Gut Project collected data from 1,375 individuals, 90% of whom were white.<a class="footnote-ref" id="fnref:99" href="#fn:99">99</a> The Healthy Life in an Urban Setting (HELIUS) study in Amsterdam found that those of Dutch ancestry had the highest level of gut microbiota diversity, while those of South Asian and <a href="/facts/Surinamese_people/9hIu90UF">Surinamese</a> descent had the lowest diversity. The study results suggested that individuals of the same race or ethnicity have more similar microbiomes than individuals of different racial backgrounds.<a class="footnote-ref" id="fnref:100" href="#fn:100">100</a>

<h3>Socioeconomic status</h3>
As of 2020, at least two studies have demonstrated a link between an individual's <a href="/facts/Socioeconomic_status/5rVhvE8b">socioeconomic status</a> (SES) and their gut microbiota. A study in <a href="/facts/Chicago/yPMokrXH">Chicago</a> found that individuals in higher SES neighborhoods had greater microbiota diversity. People from higher SES neighborhoods also had more abundant Bacteroides bacteria. Similarly, a study of <a href="/facts/Twin/9QSssff4">twins</a> in the United Kingdom found that higher SES was also linked with a greater gut diversity.<a class="footnote-ref" id="fnref:101" href="#fn:101">101</a>

<h3>Antibiotic use</h3>
As of 2023, a study suggests that antibiotics, especially those used in the treatment of broad-spectrum bacterial infections, have negative effects on the gut microbiota.<a class="footnote-ref" id="fnref:102" href="#fn:102">102</a> The study also states that there are many experts on intestinal health concerned that antibody usage has reduced the diversity of the gut microbiota, many of the strains are lost, and if there is a re-emergence of the bacteria, is gradual and long-term.<a class="footnote-ref" id="fnref:103" href="#fn:103">103</a>

<h2 id="functions">Functions</h2>
When the study of gut flora began in 1995,<a class="footnote-ref" id="fnref:104" href="#fn:104">104</a> it was thought to have three key roles: direct defense against <a href="/facts/Pathogen/axMXtV1M">pathogens</a>, fortification of host defense by its role in developing and maintaining the <a href="/facts/Intestinal_epithelium/32hWmspE">intestinal epithelium</a> and inducing antibody production there, and metabolizing otherwise indigestible compounds in food. Subsequent work discovered its role in training the developing immune system, and yet further work focused on its role in the <a href="/facts/Gut%25E2%2580%2593brain_axis/eGYP9t6d">gut–brain axis</a>.<a class="footnote-ref" id="fnref:105" href="#fn:105">105</a>
The gut microbiota not only influences intestinal health but also plays a role in systemic immune regulation, including interactions with the pulmonary immune environment through what is known as the 'gut–lung axis'.<a class="footnote-ref" id="fnref:106" href="#fn:106">106</a>

<h3>Direct inhibition of pathogens</h3>
The gut flora community plays a direct role in defending against pathogens by fully colonising the space, making use of all available nutrients, and by secreting compounds known as <a href="/facts/Cytokine/SdWpWABH">cytokines</a> that kill or inhibit unwelcome organisms that would compete for nutrients with it.<a class="footnote-ref" id="fnref:107" href="#fn:107">107</a> Different strains of gut bacteria cause the production of different cytokines. Cytokines are chemical compounds produced by our immune system for initiating the <a href="/facts/Inflammatory_response/Ura86MIy">inflammatory response</a> against infections. Disruption of the gut flora allows competing organisms like <a href="/facts/Clostridioides_difficile_(bacteria)/lELAUztP">Clostridioides difficile</a> to become established that otherwise are kept in abeyance.<a class="footnote-ref" id="fnref:108" href="#fn:108">108</a>

<h3>Development of enteric protection and immune system</h3>

Gut flora in infants becomes similar to an adult within one to two years of birth.<a class="footnote-ref" id="fnref:109" href="#fn:109">109</a> As the gut flora establishes, the lining of the intestines – the intestinal epithelium and the intestinal mucosal barrier that it secretes – develop a <a href="/facts/Symbiosis/MrBArRGa">symbiosis</a> with microorganisms.<a class="footnote-ref" id="fnref:110" href="#fn:110">110</a> Specifically, <a href="/facts/Goblet_cell/FzXnFFr1">goblet cells</a> that produce the mucosa proliferate, and the mucosa layer thickens, providing an outside mucosal layer in which favorable microorganisms can anchor and feed, and an inner layer that these organisms cannot penetrate.<a class="footnote-ref" id="fnref:111" href="#fn:111">111</a><a class="footnote-ref" id="fnref:112" href="#fn:112">112</a> Additionally, the development of <a href="/facts/Gut-associated_lymphoid_tissue/4F7GBmRL">gut-associated lymphoid tissue</a> (GALT), which forms part of the intestinal epithelium and which detects and reacts to pathogens, develops during the time that the gut flora becomes established.<a class="footnote-ref" id="fnref:113" href="#fn:113">113</a> The GALT that develops is tolerant to gut flora species, but not to other microorganisms.<a class="footnote-ref" id="fnref:114" href="#fn:114">114</a> GALT also normally becomes tolerant to food the infant consumes, and the gut flora <a href="/facts/Metabolites/nAyywVtA">metabolites</a> (molecules formed from metabolism) produced from food.<a class="footnote-ref" id="fnref:115" href="#fn:115">115</a>
The human <a href="/facts/Immune_system/HRCTf1pb">immune system</a> creates <a href="/facts/Cytokine/SdWpWABH">cytokines</a> that can drive the immune system to produce inflammation in order to protect itself, and that can tamp down the immune response to maintain <a href="/facts/Homeostasis/rloTGAHa">homeostasis</a> and allow healing after insult or injury.<a class="footnote-ref" id="fnref:116" href="#fn:116">116</a> Different bacterial species that appear in gut flora have been shown to be able to drive the immune system to create cytokines selectively; for example <a href="/facts/Bacteroides_fragilis/94ovcupK">Bacteroides fragilis</a> and some <a href="/facts/Clostridia/g3mSz5XP">Clostridia</a> species appear to drive an anti-inflammatory response, while some <a href="/facts/Segmented_filamentous_bacteria/cDp0Sz7o">segmented filamentous bacteria</a> drive the production of inflammatory cytokines.<a class="footnote-ref" id="fnref:117" href="#fn:117">117</a><a class="footnote-ref" id="fnref:118" href="#fn:118">118</a> Gut flora can also regulate the production of <a href="/facts/Antibodies/MX8pdTdP">antibodies</a> by the immune system.<a class="footnote-ref" id="fnref:119" href="#fn:119">119</a><a class="footnote-ref" id="fnref:120" href="#fn:120">120</a> One function of this regulation is to cause <a href="/facts/B_cells/6Y1tgwwp">B cells</a> to class switch to <a href="/facts/IgA/G0HzhnWt">IgA</a>. In most cases B cells need activation from <a href="/facts/T_helper_cells/nhwAYkDj">T helper cells</a> to induce <a href="/facts/Class_switching/q8w8PWoY">class switching</a>; however, in another pathway, gut flora cause <a href="/facts/NF-kB/qcpt5vuQ">NF-kB</a> signaling by intestinal epithelial cells which results in further signaling molecules being secreted.<a class="footnote-ref" id="fnref:121" href="#fn:121">121</a> These signaling molecules interact with B cells to induce class switching to IgA.<a class="footnote-ref" id="fnref:122" href="#fn:122">122</a> IgA is an important type of antibody that is used in mucosal environments like the gut. It has been shown that IgA can help diversify the gut community and helps in getting rid of bacteria that cause inflammatory responses.<a class="footnote-ref" id="fnref:123" href="#fn:123">123</a> Ultimately, IgA maintains a healthy environment between the host and gut bacteria.<a class="footnote-ref" id="fnref:124" href="#fn:124">124</a> These cytokines and antibodies can have effects outside the gut, in the lungs and other tissues.<a class="footnote-ref" id="fnref:125" href="#fn:125">125</a>
A 2022 review indicated that various mechanisms are under preliminary research to assess how gut microbes may modulate <a href="/facts/Vaccine_immunogenicity/QVxzK4tD">vaccine immunogenicity</a>, including effects on <a href="/facts/Antigen_presentation/RMEAcYwR">antigen presentation</a> and cytokine profiles.<a class="footnote-ref" id="fnref:126" href="#fn:126">126</a>

<h3>Metabolism</h3>
<table><tbody><tr><td></td></tr></tbody></table>
Without gut flora, the human body would be unable to utilize some of the undigested <a href="/facts/Carbohydrate/Geuuzxsf">carbohydrates</a> it consumes, because some types of gut flora have <a href="/facts/Enzyme/DSI1Fh7y">enzymes</a> that human cells lack for breaking down certain <a href="/facts/Polysaccharide/lqXq2cJU">polysaccharides</a>.<a class="footnote-ref" id="fnref:127" href="#fn:127">127</a> Rodents raised in a <a href="/facts/Asepsis/LwhPKr7d">sterile</a> environment and lacking in gut flora need to eat 30% more <a href="/facts/Calorie_(food)/TtuzDgbX">calories</a> just to remain the same weight as their normal counterparts.<a class="footnote-ref" id="fnref:128" href="#fn:128">128</a> Carbohydrates that humans cannot <a href="/facts/Digestion/sjUBmhBS">digest</a> without bacterial help include certain <a href="/facts/Starch_(food)/gHAqGfJb">starches</a>, <a href="/facts/Fiber_(food)/Q9DXanDv">fiber</a>, <a href="/facts/Oligosaccharides/5to180o3">oligosaccharides</a>, and <a href="/facts/Sugar/jb5KXRHT">sugars</a> that the body failed to digest and absorb like <a href="/facts/Lactose/lBa5ozYk">lactose</a> in the case of <a href="/facts/Lactose_intolerance/sD6q8shx">lactose intolerance</a> and <a href="/facts/Sugar_alcohol/kV7Uul59">sugar alcohols</a>, <a href="/facts/Mucus/hnlBuHAy">mucus</a> produced by the gut, and proteins.<a class="footnote-ref" id="fnref:129" href="#fn:129">129</a><a class="footnote-ref" id="fnref:130" href="#fn:130">130</a>
Bacteria turn carbohydrates they ferment into <a href="/facts/Short-chain_fatty_acid/bgj2XGRf">short-chain fatty acids</a> by a form of fermentation called saccharolytic fermentation.<a class="footnote-ref" id="fnref:131" href="#fn:131">131</a> Products include <a href="/facts/Acetic_acid/uyBKA2Pd">acetic acid</a>, <a href="/facts/Propionic_acid/ugBEw0Ia">propionic acid</a> and <a href="/facts/Butyric_acid/Sy5NrhK5">butyric acid</a>.<a class="footnote-ref" id="fnref:132" href="#fn:132">132</a><a class="footnote-ref" id="fnref:133" href="#fn:133">133</a> These materials can be used by host cells, providing a major source of energy and nutrients.<a class="footnote-ref" id="fnref:134" href="#fn:134">134</a> Gases (which are involved in <a href="/facts/Gaseous_signaling_molecules/BxUDv71M">signaling</a><a class="footnote-ref" id="fnref:135" href="#fn:135">135</a> and may cause <a href="/facts/Flatulence/XMAcIUru">flatulence</a>) and <a href="/facts/Organic_acid/2Pfb26Lp">organic acids</a>, such as <a href="/facts/Lactic_acid/BsVRFx7s">lactic acid</a>, are also produced by fermentation.<a class="footnote-ref" id="fnref:136" href="#fn:136">136</a> Acetic acid is used by <a href="/facts/Muscle/dmxrL8pH">muscle</a>, propionic acid facilitates <a href="/facts/Liver/Rtp4Fk2b">liver</a> production of <a href="/facts/Adenosine_triphosphate/nB9bwgcU">ATP</a>, and butyric acid provides energy to gut cells.<a class="footnote-ref" id="fnref:137" href="#fn:137">137</a>
Gut flora also synthesize vitamins like <a href="/facts/Biotin/WAaVxyB7">biotin</a> and <a href="/facts/Folate/8Eb7An6D">folate</a>, and facilitate absorption of <a href="/facts/Dietary_minerals/ACv8EG7f">dietary minerals</a>, including magnesium, calcium, and iron.<a class="footnote-ref" id="fnref:138" href="#fn:138">138</a><a class="footnote-ref" id="fnref:139" href="#fn:139">139</a> <a href="/facts/Methanobrevibacter_smithii/GK0TTAQJ">Methanobrevibacter smithii</a> is unique because it is not a species of bacteria, but rather a member of <a href="/facts/Domain_(taxonomy)/RpP6V7n6">domain</a> <a href="/facts/Archaea/Adxh0aHw">Archaea</a>, and is the most abundant <a href="/facts/Methane/kBHneYnh">methane</a>-producing archaeal species in the human gastrointestinal microbiota.<a class="footnote-ref" id="fnref:140" href="#fn:140">140</a>
Gut microbiota also serve as a source of vitamins K and B12, which are not produced by the body or produced in little amount.<a class="footnote-ref" id="fnref:141" href="#fn:141">141</a><a class="footnote-ref" id="fnref:142" href="#fn:142">142</a>

<h4>Cellulose degradation</h4>
Bacteria that degrade cellulose (such as <a href="/facts/Ruminococcus/bl6a6t0p">Ruminococcus</a>) are prevalent among <a href="/facts/Hominidae/ILn1SYKB">great apes</a>, ancient human societies, <a href="/facts/Hunter-gatherer/ghnjoNbJ">hunter-gatherer</a> communities, and even modern rural populations. However, they are rare in industrialized societies. Human-associated strains have acquired genes that can degrade specific plant fibers such as <a href="/facts/Maize/lJ6c5xMH">maize</a>, <a href="/facts/Rice/wvL1hBCz">rice</a>, and <a href="/facts/Wheat/lrk6HdV3">wheat</a>. Bacterial strains found in primates can also degrade <a href="/facts/Chitin/Fo1f8b86">chitin</a>, a polymer abundant in insects, which are part of the diet of many nonhuman <a href="/facts/Primate/Hl8RNE2X">primates</a>. The decline of these bacteria in the human gut were likely influenced by the shift toward western lifestyles.<a class="footnote-ref" id="fnref:143" href="#fn:143">143</a>

<h4>Pharmacomicrobiomics</h4>
The human <a href="/facts/Metagenomics/GWFeMd7z">metagenome</a> (i.e., the genetic composition of an individual and all microorganisms that reside on or within the individual's body) varies considerably between individuals.<a class="footnote-ref" id="fnref:144" href="#fn:144">144</a><a class="footnote-ref" id="fnref:145" href="#fn:145">145</a> Since the total number of microbial cells in the human body (over 100 trillion) greatly outnumbers Homo sapiens cells (tens of trillions),<a class="footnote-ref" id="fnref:146" href="#fn:146">146</a><a class="footnote-ref" id="fnref:147" href="#fn:147">147</a><a class="footnote-ref" id="fnref:148" href="#fn:148">148</a> there is considerable potential for interactions between drugs and an individual's microbiome, including: drugs altering the composition of the <a href="/facts/Human_microbiome/xJIRMUAY">human microbiome</a>, <a href="/facts/Drug_metabolism/I5nQ28Ma">drug metabolism</a> by microbial enzymes modifying the drug's <a href="/facts/Pharmacokinetic/x4CUUnle">pharmacokinetic</a> profile, and microbial drug metabolism affecting a drug's clinical efficacy and <a href="/facts/Toxicity/qa96rs60">toxicity</a> profile.<a class="footnote-ref" id="fnref:149" href="#fn:149">149</a><a class="footnote-ref" id="fnref:150" href="#fn:150">150</a><a class="footnote-ref" id="fnref:151" href="#fn:151">151</a>
Apart from carbohydrates, gut microbiota can also metabolize other <a href="/facts/Xenobiotic/0M2LAyEx">xenobiotics</a> such as drugs, <a href="/facts/Phytochemical/Txrr3QVx">phytochemicals</a>, and food toxicants. More than 30 drugs have been shown to be metabolized by gut microbiota.<a class="footnote-ref" id="fnref:152" href="#fn:152">152</a> The microbial metabolism of drugs can sometimes inactivate the drug.<a class="footnote-ref" id="fnref:153" href="#fn:153">153</a>

<h5>Contribution to drug metabolism</h5>
The gut microbiota is an enriched community that contains diverse genes with huge biochemical capabilities to modify drugs, especially those taken by mouth.<a class="footnote-ref" id="fnref:154" href="#fn:154">154</a> Gut microbiota can affect drug metabolism via direct and indirect mechanisms.<a class="footnote-ref" id="fnref:155" href="#fn:155">155</a> The direct mechanism is mediated by the microbial enzymes that can modify the chemical structure of the administered drugs.<a class="footnote-ref" id="fnref:156" href="#fn:156">156</a> Conversely, the indirect pathway is mediated by the microbial metabolites which affect the expression of host metabolizing enzymes such as <a href="/facts/Cytochrome_P450/alxusFD0">cytochrome P450</a>.<a class="footnote-ref" id="fnref:157" href="#fn:157">157</a><a class="footnote-ref" id="fnref:158" href="#fn:158">158</a> The effects of the gut microbiota on the pharmacokinetics and bioavailability of the drug have been investigated a few decades ago.<a class="footnote-ref" id="fnref:159" href="#fn:159">159</a><a class="footnote-ref" id="fnref:160" href="#fn:160">160</a><a class="footnote-ref" id="fnref:161" href="#fn:161">161</a> These effects can be varied; it could activate the inactive drugs such as lovastatin,<a class="footnote-ref" id="fnref:162" href="#fn:162">162</a> inactivate the active drug such as <a href="/facts/Digoxin/JEHbskXq">digoxin</a><a class="footnote-ref" id="fnref:163" href="#fn:163">163</a> or induce drug toxicity as in <a href="/facts/Irinotecan/k6KbGLG0">irinotecan</a>.<a class="footnote-ref" id="fnref:164" href="#fn:164">164</a> Since then, the impacts of the gut microbiota on the pharmacokinetics of many drugs were heavily studied.<a class="footnote-ref" id="fnref:165" href="#fn:165">165</a><a class="footnote-ref" id="fnref:166" href="#fn:166">166</a>
The human gut microbiota plays a crucial role in modulating the effect of the administered drugs on the human. Directly, gut microbiota can synthesize and release a series of enzymes with the capability to metabolize drugs such as microbial biotransformation of L-dopa by decarboxylase and dehydroxylase enzymes.<a class="footnote-ref" id="fnref:167" href="#fn:167">167</a> On the contrary, gut microbiota may also alter the metabolism of the drugs by modulating the host drug metabolism. This mechanism can be mediated by microbial metabolites or by modifying host metabolites which in turn change the expression of host metabolizing enzymes.<a class="footnote-ref" id="fnref:168" href="#fn:168">168</a>
A large number of studies have demonstrated the metabolism of over 50 drugs by the gut microbiota.<a class="footnote-ref" id="fnref:169" href="#fn:169">169</a><a class="footnote-ref" id="fnref:170" href="#fn:170">170</a> For example, lovastatin (a cholesterol-lowering agent) which is a lactone prodrug is partially activated by the human gut microbiota forming active acid hydroxylated metabolites.<a class="footnote-ref" id="fnref:171" href="#fn:171">171</a> Conversely, digoxin (a drug used to treat Congestive Heart Failure) is inactivated by a member of the gut microbiota (i.e. Eggerthella lanta).<a class="footnote-ref" id="fnref:172" href="#fn:172">172</a> Eggerthella lanta has a cytochrome-encoding operon up-regulated by digoxin and associated with digoxin-inactivation.<a class="footnote-ref" id="fnref:173" href="#fn:173">173</a> Gut microbiota can also modulate the efficacy and toxicity of chemotherapeutic agents such as irinotecan.<a class="footnote-ref" id="fnref:174" href="#fn:174">174</a> This effect is derived from the microbiome-encoded β-glucuronidase enzymes which recover the active form of the irinotecan causing gastrointestinal toxicity.<a class="footnote-ref" id="fnref:175" href="#fn:175">175</a>

<h5>Secondary metabolites</h5>
This microbial community in the gut has a huge biochemical capability to produce distinct secondary metabolites that are sometimes produced from the metabolic conversion of dietary foods such as <a href="/facts/Fiber/ttkxAFBu">fibers</a>, endogenous biological compounds such as <a href="/facts/Indole/HT72P6e6">indole</a> or <a href="/facts/Bile_acid/ojTJzf0c">bile acids</a>.<a class="footnote-ref" id="fnref:176" href="#fn:176">176</a><a class="footnote-ref" id="fnref:177" href="#fn:177">177</a><a class="footnote-ref" id="fnref:178" href="#fn:178">178</a> Microbial metabolites especially short chain fatty acids (SCFAs) and secondary bile acids (BAs) play important roles for the human in health and disease states.<a class="footnote-ref" id="fnref:179" href="#fn:179">179</a><a class="footnote-ref" id="fnref:180" href="#fn:180">180</a><a class="footnote-ref" id="fnref:181" href="#fn:181">181</a>
One of the most important bacterial metabolites produced by the gut microbiota is secondary bile acids (BAs).<a class="footnote-ref" id="fnref:182" href="#fn:182">182</a> These metabolites are produced by the bacterial biotransformation of the primary bile acids such as cholic acid (CA) and chenodeoxycholic acid (CDCA) into secondary bile acids (BAs) lithocholic acid (LCA) and deoxy cholic acid (DCA) respectively.<a class="footnote-ref" id="fnref:183" href="#fn:183">183</a> Primary bile acids which are synthesized by hepatocytes and stored in the gall bladder possess hydrophobic characters. These metabolites are subsequently metabolized by the gut microbiota into secondary metabolites with increased hydrophobicity.<a class="footnote-ref" id="fnref:184" href="#fn:184">184</a> Bile salt hydrolases (BSH) which are conserved across gut microbiota phyla such as Bacteroides, Firmicutes, and Actinobacteria responsible for the first step of secondary bile acids metabolism.<a class="footnote-ref" id="fnref:185" href="#fn:185">185</a> Secondary bile acids (BAs) such as DCA and LCA have been demonstrated to inhibit both Clostridioides difficile germination and outgrowth.<a class="footnote-ref" id="fnref:186" href="#fn:186">186</a>

<h4>Dysbiosis</h4>
The gut microbiota is important for maintaining homeostasis in the intestine. Development of <a href="/facts/Gastrointestinal_cancer/JyWWkwmg">intestinal cancer</a> is associated with an imbalance in the natural microflora (dysbiosis).<a class="footnote-ref" id="fnref:187" href="#fn:187">187</a> The secondary bile acid <a href="/facts/Deoxycholic_acid/FeINsvla">deoxycholic acid</a> is associated with alterations of the microbial community that lead to increased intestinal carcinogenesis.<a class="footnote-ref" id="fnref:188" href="#fn:188">188</a> Increased exposure of the colon to secondary bile acids resulting from dysbiosis can cause <a href="/facts/DNA_damage_(naturally_occurring)/CjGTLKGl">DNA damage</a>, and such damage can produce carcinogenic mutations in cells of the colon.<a class="footnote-ref" id="fnref:189" href="#fn:189">189</a> The high density of bacteria in the <a href="/facts/Colon_(anatomy)/vQtlNBv9">colon</a> (about 1012 per ml.) that are subject to dysbiosis compared to the relatively low density in the <a href="/facts/Small_intestine/1AQ8RJ4m">small intestine</a> (about 102 per ml.) may account for the greater than 10-fold higher incidence of cancer in the colon compared to the small intestine.<a class="footnote-ref" id="fnref:190" href="#fn:190">190</a>

<h3>Gut–brain axis</h3>
Main article: <a href="/facts/Gut%25E2%2580%2593brain_axis/eGYP9t6d">Gut–brain axis</a>
The gut microbiota contributes to digestion and immune modulation, as it plays a role in the gut-brain axis, where microbial metabolites such as short-chain fatty acids and neurotransmitters influence brain function and behavior. The gut–brain axis is the biochemical signaling that takes place between the <a href="/facts/Gastrointestinal_tract/nK2zwqBS">gastrointestinal tract</a> and the <a href="/facts/Central_nervous_system/k8I6To97">central nervous system</a>.<a class="footnote-ref" id="fnref:191" href="#fn:191">191</a> That term has been expanded to include the role of the gut flora in the interplay; the term "microbiome––brain axis" is sometimes used to describe paradigms explicitly including the gut flora.<a class="footnote-ref" id="fnref:192" href="#fn:192">192</a><a class="footnote-ref" id="fnref:193" href="#fn:193">193</a><a class="footnote-ref" id="fnref:194" href="#fn:194">194</a> Broadly defined, the gut-brain axis includes the central nervous system, <a href="/facts/Neuroendocrine_System/lVldJ7MB">neuroendocrine</a> and <a href="/facts/Neuroimmune_system/6vy1P5cW">neuroimmune</a> systems including the <a href="/facts/Hypothalamic%25E2%2580%2593pituitary%25E2%2580%2593adrenal_axis/062CevaI">hypothalamic–pituitary–adrenal axis</a> (HPA axis), sympathetic and parasympathetic arms of the <a href="/facts/Autonomic_nervous_system/hdmEY1Ay">autonomic nervous system</a> including the <a href="/facts/Enteric_nervous_system/W6U5L9s5">enteric nervous system</a>, the <a href="/facts/Vagus_nerve/cKQR0rLm">vagus nerve</a>, and the gut <a href="/facts/Microbiota/V4ymrawz">microbiota</a>.<a class="footnote-ref" id="fnref:195" href="#fn:195">195</a><a class="footnote-ref" id="fnref:196" href="#fn:196">196</a>
A 2016 <a href="/facts/Systematic_review/dGvq3BGx">systematic review</a> of preclinical studies and small human trials conducted with certain commercially available strains of probiotic bacteria found that <a href="/facts/Bifidobacterium/ov3Sghxb">Bifidobacterium</a> and Lactobacillus <a href="/facts/Genera/m8EFjSms">genera</a> (<a href="/facts/B._longum/bkUFIBaJ">B. longum</a>, <a href="/facts/B._breve/e0L58kL4">B. breve</a>, <a href="/facts/B._infantis/bkUFIBaJ">B. infantis</a>, <a href="/facts/L._helveticus/rUFvJgmu">L. helveticus</a>, <a href="/facts/L._rhamnosus/msxVquT6">L. rhamnosus</a>, <a href="/facts/Lactobacillus_plantarum/FSsX66vv">L. plantarum</a>, and <a href="/facts/L._casei/lnSQ1BHg">L. casei</a>), were of interest for certain <a href="/facts/Central_nervous_system_disorder/EGlB2D4w">central nervous system disorders</a>.<a class="footnote-ref" id="fnref:197" href="#fn:197">197</a>

<h2 id="alterations-in-microbiota-balance">Alterations in microbiota balance</h2>
<h3>Effects of antibiotic use</h3>
Altering the numbers of gut bacteria, for example by taking <a href="/facts/Broad-spectrum_antibiotic/gITH5ecM">broad-spectrum antibiotics</a>, may affect the host's health and ability to digest food.<a class="footnote-ref" id="fnref:198" href="#fn:198">198</a> Antibiotics can cause <a href="/facts/Antibiotic-associated_diarrhea/hlzEWfBJ">antibiotic-associated diarrhea</a> by irritating the <a href="/facts/Bowel/nK2zwqBS">bowel</a> directly, changing the levels of microbiota, or allowing <a href="/facts/Pathogen/axMXtV1M">pathogenic</a> bacteria to grow.<a class="footnote-ref" id="fnref:199" href="#fn:199">199</a> Another harmful effect of antibiotics is the increase in numbers of <a href="/facts/Antibiotic-resistant_bacteria/jsbAywgx">antibiotic-resistant bacteria</a> found after their use, which, when they invade the host, cause illnesses that are difficult to treat with antibiotics.<a class="footnote-ref" id="fnref:200" href="#fn:200">200</a>
Changing the numbers and species of gut microbiota can reduce the body's ability to ferment carbohydrates and metabolize <a href="/facts/Bile/7c5ufDao">bile</a> acids and may cause <a href="/facts/Diarrhea/6TBHaRdA">diarrhea</a>. Carbohydrates that are not broken down may absorb too much water and cause runny stools, or lack of SCFAs produced by gut microbiota could cause diarrhea.<a class="footnote-ref" id="fnref:201" href="#fn:201">201</a>
A reduction in levels of native bacterial species also disrupts their ability to inhibit the growth of harmful species such as C. difficile and Salmonella Kedougou, and these species can get out of hand, though their overgrowth may be incidental and not be the true cause of diarrhea.<a class="footnote-ref" id="fnref:202" href="#fn:202">202</a><a class="footnote-ref" id="fnref:203" href="#fn:203">203</a><a class="footnote-ref" id="fnref:204" href="#fn:204">204</a> Emerging treatment protocols for C. difficile infections involve fecal microbiota transplantation of donor feces (see <a href="/facts/Fecal_transplant/XX5Ytk9g">Fecal transplant</a>).<a class="footnote-ref" id="fnref:205" href="#fn:205">205</a> Initial reports of treatment describe success rates of 90%, with few side effects. Efficacy is speculated to result from restoring bacterial balances of bacteroides and firmicutes classes of bacteria.<a class="footnote-ref" id="fnref:206" href="#fn:206">206</a>
The composition of the gut microbiome also changes in severe illnesses, due not only to antibiotic use but also to such factors as <a href="/facts/Ischemia/ySL9xbCl">ischemia</a> of the gut, failure to eat, and <a href="/facts/Immune_compromise/CIEujXmc">immune compromise</a>. Negative effects from this have led to interest in selective digestive tract decontamination, a treatment to kill only pathogenic bacteria and allow the re-establishment of healthy ones.<a class="footnote-ref" id="fnref:207" href="#fn:207">207</a>
Antibiotics alter the population of the microbiota in the <a href="/facts/Gastrointestinal_tract/nK2zwqBS">gastrointestinal tract</a>, and this may change the intra-community metabolic interactions, modify caloric intake by using carbohydrates, and globally affect host metabolic, hormonal, and immune homeostasis.<a class="footnote-ref" id="fnref:208" href="#fn:208">208</a>
There is reasonable evidence that taking probiotics containing Lactobacillus species may help prevent antibiotic-associated diarrhea and that taking probiotics with Saccharomyces (e.g., <a href="/facts/Saccharomyces_boulardii/GFsuF5M0">Saccharomyces boulardii</a> ) may help to prevent Clostridioides difficile infection following systemic antibiotic treatment.<a class="footnote-ref" id="fnref:209" href="#fn:209">209</a>

<h3>Pregnancy</h3>
The gut microbiota of a woman changes as <a href="/facts/Pregnancy/vEKYGpep">pregnancy</a> advances, with the changes similar to those seen in <a href="/facts/Metabolic_syndromes/jI70tRBv">metabolic syndromes</a> such as diabetes. The change in gut microbiota causes no ill effects. The newborn's gut microbiota resemble the mother's first-trimester samples. The diversity of the microbiome decreases from the first to third trimester, as the numbers of certain species go up.<a class="footnote-ref" id="fnref:210" href="#fn:210">210</a><a class="footnote-ref" id="fnref:211" href="#fn:211">211</a>

<h3>Probiotics, prebiotics, synbiotics, and pharmabiotics</h3>
<a href="/facts/Probiotics/gQNAN6ly">Probiotics</a> contain live <a href="/facts/Microorganism/pysJYcE2">microorganisms</a>. When consumed, they are believed to provide health benefits by altering the microbiome composition.<a class="footnote-ref" id="fnref:212" href="#fn:212">212</a><a class="footnote-ref" id="fnref:213" href="#fn:213">213</a><a class="footnote-ref" id="fnref:214" href="#fn:214">214</a> Current research explores using probiotics as a way to restore the microbial balance of the <a href="/facts/Gastrointestinal_tract/nK2zwqBS">intestine</a> by stimulating the immune system and inhibiting pro-inflammatory <a href="/facts/Cytokine/SdWpWABH">cytokines</a>.<a class="footnote-ref" id="fnref:215" href="#fn:215">215</a>
With regard to gut microbiota, <a href="/facts/Prebiotic_(nutrition)/mHlPFE2k">prebiotics</a> are typically non-digestible, <a href="/facts/Dietary_fiber/Q9DXanDv">fiber</a> compounds that pass undigested through the upper part of the <a href="/facts/Gastrointestinal_tract/nK2zwqBS">gastrointestinal tract</a> and stimulate the growth or activity of advantageous gut flora by acting as <a href="/facts/Substrate_(biology)/EBDd458H">substrate</a> for them.<a class="footnote-ref" id="fnref:216" href="#fn:216">216</a><a class="footnote-ref" id="fnref:217" href="#fn:217">217</a>
<a href="/facts/Synbiotics/XdCHaK1S">Synbiotics</a> refers to <a href="/facts/Food_ingredient/llUca77D">food ingredients</a> or <a href="/facts/Dietary_supplements/SHXNNxaS">dietary supplements</a> combining probiotics and prebiotics in a form of <a href="/facts/Synergy/lfcwWuAc">synergism</a>.<a class="footnote-ref" id="fnref:218" href="#fn:218">218</a>
The term "pharmabiotics" is used in various ways, to mean: <a href="/facts/Pharmaceutical_formulation/lH90KTRq">pharmaceutical formulations</a> (standardized manufacturing that can obtain regulatory approval as a drug) of probiotics, <a href="/facts/Prebiotic_(nutrition)/mHlPFE2k">prebiotics</a>, or <a href="/facts/Synbiotics/XdCHaK1S">synbiotics</a>;<a class="footnote-ref" id="fnref:219" href="#fn:219">219</a> probiotics that have been genetically engineered or otherwise optimized for best performance (shelf life, survival in the digestive tract, etc.);<a class="footnote-ref" id="fnref:220" href="#fn:220">220</a> and the natural products of gut flora metabolism (vitamins, etc.).<a class="footnote-ref" id="fnref:221" href="#fn:221">221</a>
There is some evidence that treatment with some probiotic strains of bacteria may be effective in treatment of <a href="/facts/Irritable_bowel_syndrome/FW24EYbP">irritable bowel syndrome</a>, <a href="/facts/Inflammatory_bowel_disease/RuxcPW5A">inflammatory bowel disease</a>, and <a href="/facts/Bloating/GnjG2Mdz">abdominal bloating</a>.<a class="footnote-ref" id="fnref:222" href="#fn:222">222</a><a class="footnote-ref" id="fnref:223" href="#fn:223">223</a><a class="footnote-ref" id="fnref:224" href="#fn:224">224</a><a class="footnote-ref" id="fnref:225" href="#fn:225">225</a> Those organisms most likely to result in a decrease of symptoms have included:

<ul><li><a href="/facts/Bifidobacterium_breve/e0L58kL4">Bifidobacterium breve</a></li>
<li><a href="/facts/Bifidobacterium_infantis/bkUFIBaJ">Bifidobacterium infantis</a></li>
<li><a href="/facts/Enterococcus_faecium/Ek2mFsQP">Enterococcus faecium</a></li>
<li><a href="/facts/Lactobacillus_plantarum/FSsX66vv">Lactobacillus plantarum</a></li>
<li><a href="/facts/Lactobacillus_reuteri/GjEPSPQo">Lactobacillus reuteri</a></li>
<li><a href="/facts/Lactobacillus_rhamnosus/msxVquT6">Lactobacillus rhamnosus</a></li>
<li><a href="/facts/Lactobacillus_salivarius/e49DCU3Q">Lactobacillus salivarius</a></li>
<li><a href="/facts/Propionibacterium_freudenreichii/Mqf9MEXy">Propionibacterium freudenreichii</a></li>
<li><a href="/facts/Saccharomyces_boulardii/GFsuF5M0">Saccharomyces boulardii</a></li>
<li><a href="/facts/Escherichia_coli_Nissle_1917/V8D7pm5G">Escherichia coli Nissle 1917</a></li>
<li><a href="/facts/Streptococcus_thermophilus/DtvWNME6">Streptococcus thermophilus</a></li></ul>
<h3>Research</h3>
Tests for whether non-antibiotic drugs may impact human gut-associated bacteria were performed by <a href="/facts/In_vitro/evp3hAX6">in vitro</a> analysis on more than 1000 marketed drugs against 40 gut bacterial strains, demonstrating that 24% of the drugs inhibited the growth of at least one of the bacterial strains.<a class="footnote-ref" id="fnref:226" href="#fn:226">226</a>

<h2 id="role-in-disease">Role in disease</h2>
Bacteria in the digestive tract can contribute to and be affected by disease in various ways. The presence or overabundance of some kinds of bacteria may contribute to inflammatory disorders such as <a href="/facts/Inflammatory_bowel_disease/RuxcPW5A">inflammatory bowel disease</a>.<a class="footnote-ref" id="fnref:227" href="#fn:227">227</a> Additionally, metabolites from certain members of the gut flora may influence host signalling pathways, contributing to disorders such as <a href="/facts/Obesity/RBF9y5Vl">obesity</a> and <a href="/facts/Colon_cancer/nV592sW7">colon cancer</a>.<a class="footnote-ref" id="fnref:228" href="#fn:228">228</a> Some gut bacteria may also cause <a href="/facts/Infection/182XrncP">infections</a> and <a href="/facts/Sepsis/n52bkffJ">sepsis</a>, for example when they are allowed to <a href="/facts/Intestinal_permeability/zQThl74p">pass from the gut into the rest of the body</a>.<a class="footnote-ref" id="fnref:229" href="#fn:229">229</a>

<h3>Ulcers</h3>
<a href="/facts/Helicobacter_pylori/9q4H68LP">Helicobacter pylori</a> infection can initiate formation of stomach ulcers when the bacteria penetrate the stomach epithelial lining, then causing an <a href="/facts/Phagocytosis/eBrv2XKV">inflammatory phagocytotic response</a>.<a class="footnote-ref" id="fnref:230" href="#fn:230">230</a> In turn, the inflammation damages parietal cells which release excessive <a href="/facts/Hydrochloric_acid/HqItJlUT">hydrochloric acid</a> into the stomach and produce less of the protective mucus.<a class="footnote-ref" id="fnref:231" href="#fn:231">231</a> Injury to the stomach lining, leading to <a href="/facts/Stomach_ulcer/peMGnYCd">ulcers</a>, develops when gastric acid overwhelms the defensive properties of cells and inhibits endogenous <a href="/facts/Prostaglandin/kIKw0gDj">prostaglandin</a> synthesis, reduces mucus and bicarbonate secretion, reduces mucosal blood flow, and lowers resistance to injury.<a class="footnote-ref" id="fnref:232" href="#fn:232">232</a> Reduced protective properties of the stomach lining increase vulnerability to further injury and ulcer formation by stomach acid, <a href="/facts/Pepsin/pELlV241">pepsin</a>, and bile salts.<a class="footnote-ref" id="fnref:233" href="#fn:233">233</a><a class="footnote-ref" id="fnref:234" href="#fn:234">234</a>

<h3>Bowel perforation</h3>
Normally-<a href="/facts/Commensalism/KnJkboX0">commensal bacteria</a> can harm the host if they extrude from the intestinal tract.<a class="footnote-ref" id="fnref:235" href="#fn:235">235</a><a class="footnote-ref" id="fnref:236" href="#fn:236">236</a> Translocation, which occurs when bacteria leave the gut through its <a href="/facts/Mucosa/oIw0vyel">mucosal</a> lining, can occur in a number of different diseases.<a class="footnote-ref" id="fnref:237" href="#fn:237">237</a> If the gut is perforated, bacteria invade the <a href="/facts/Interstitium/BBn1mz9G">interstitium</a>, causing a potentially fatal <a href="/facts/Infection/182XrncP">infection</a>.<a class="footnote-ref" id="fnref:238" href="#fn:238">238</a>: 715 

<h3>Inflammatory bowel diseases</h3>
The two main types of <a href="/facts/Inflammatory_bowel_disease/RuxcPW5A">inflammatory bowel diseases</a>, <a href="/facts/Crohn%2527s_disease/zm55cBtd">Crohn's disease</a> and <a href="/facts/Ulcerative_colitis/BIkyFzRj">ulcerative colitis</a>, are <a href="/facts/Chronic_condition/6CqLP41r">chronic</a> inflammatory disorders of the gut; the causes of these diseases are unknown and issues with the gut flora and its relationship with the host have been implicated in these conditions.<a class="footnote-ref" id="fnref:239" href="#fn:239">239</a><a class="footnote-ref" id="fnref:240" href="#fn:240">240</a><a class="footnote-ref" id="fnref:241" href="#fn:241">241</a><a class="footnote-ref" id="fnref:242" href="#fn:242">242</a> Additionally, it appears that interactions of gut flora with the gut–brain axis have a role in IBD, with physiological stress mediated through the <a href="/facts/Hypothalamic%25E2%2580%2593pituitary%25E2%2580%2593adrenal_axis/062CevaI">hypothalamic–pituitary–adrenal axis</a> driving changes to intestinal epithelium and the gut flora in turn releasing factors and metabolites that trigger signaling in the <a href="/facts/Enteric_nervous_system/W6U5L9s5">enteric nervous system</a> and the <a href="/facts/Vagus_nerve/cKQR0rLm">vagus nerve</a>.<a class="footnote-ref" id="fnref:243" href="#fn:243">243</a>
The diversity of gut flora appears to be significantly diminished in people with inflammatory bowel diseases compared to healthy people; additionally, in people with ulcerative colitis, Proteobacteria and Actinobacteria appear to dominate; in people with Crohn's, <a href="/facts/Enterococcus_faecium/Ek2mFsQP">Enterococcus faecium</a> and several Proteobacteria appear to be over-represented.<a class="footnote-ref" id="fnref:244" href="#fn:244">244</a>
There is reasonable evidence that correcting gut flora imbalances by taking probiotics with <a href="/facts/Lactobacilli/uKhIxU67">Lactobacilli</a> and Bifidobacteria can reduce visceral pain and gut inflammation in IBD.<a class="footnote-ref" id="fnref:245" href="#fn:245">245</a>

<h3>Irritable bowel syndrome</h3>
<a href="/facts/Irritable_bowel_syndrome/FW24EYbP">Irritable bowel syndrome</a> is a result of stress and chronic activation of the HPA axis; its symptoms include abdominal pain, changes in bowel movements, and an increase in proinflammatory cytokines. Overall, studies have found that the luminal and mucosal microbiota are changed in irritable bowel syndrome individuals, and these changes can relate to the type of irritation such as diarrhea or <a href="/facts/Constipation/l4DHHM6L">constipation</a>. Also, there is a decrease in the diversity of the microbiome with low levels of fecal Lactobacilli and Bifidobacteria, high levels of facultative <a href="/facts/Anaerobic_bacteria/bhQnlqCq">anaerobic bacteria</a> such as <a href="/facts/Escherichia_coli/nR4Gvl56">Escherichia coli</a>, and increased ratios of Firmicutes: Bacteroidetes.<a class="footnote-ref" id="fnref:246" href="#fn:246">246</a>

<h4>Asthma</h4>
With asthma, two hypotheses have been posed to explain its rising prevalence in the developed world. The <a href="/facts/Hygiene_hypothesis/3pmIpBDc">hygiene hypothesis</a> posits that children in the developed world are not exposed to enough microbes and thus may contain lower prevalence of specific bacterial taxa that play protective roles.<a class="footnote-ref" id="fnref:247" href="#fn:247">247</a> The second hypothesis focuses on the <a href="/facts/Western_pattern_diet/6fdL7lIc">Western pattern diet</a>, which lacks <a href="/facts/Whole_grain/arLz8FWD">whole grains</a> and <a href="/facts/Dietary_fiber/Q9DXanDv">fiber</a> and has an overabundance of <a href="/facts/Simple_sugars/yzs2d6Eq">simple sugars</a>.<a class="footnote-ref" id="fnref:248" href="#fn:248">248</a> Both hypotheses converge on the role of short-chain fatty acids (SCFAs) in <a href="/facts/Immunotherapy/hgq3KQaJ">immunomodulation</a>. These bacterial fermentation metabolites are involved in immune signalling that prevents the triggering of asthma and lower SCFA levels are associated with the disease.<a class="footnote-ref" id="fnref:249" href="#fn:249">249</a><a class="footnote-ref" id="fnref:250" href="#fn:250">250</a> Lacking protective genera such as Lachnospira, <a href="/facts/Veillonella/4oaT892T">Veillonella</a>, <a href="/facts/Rothia_(bacterium)/LcD2mbwy">Rothia</a> and <a href="/facts/Faecalibacterium/pyweMtzx">Faecalibacterium</a> has been linked to reduced SCFA levels.<a class="footnote-ref" id="fnref:251" href="#fn:251">251</a> Further, SCFAs are the product of bacterial fermentation of fiber, which is low in the Western pattern diet.<a class="footnote-ref" id="fnref:252" href="#fn:252">252</a><a class="footnote-ref" id="fnref:253" href="#fn:253">253</a> SCFAs offer a link between gut flora and immune disorders, and as of 2016, this was an active area of research.<a class="footnote-ref" id="fnref:254" href="#fn:254">254</a> Similar hypotheses have also been posited for the rise of food and other allergies.<a class="footnote-ref" id="fnref:255" href="#fn:255">255</a>

<h4>Diabetes mellitus type 1</h4>
The connection between the gut microbiota and <a href="/facts/Diabetes_mellitus_type_1/IkuQadGx">diabetes mellitus type 1</a> has also been linked to SCFAs, such as <a href="/facts/Butyrate/Sy5NrhK5">butyrate</a> and acetate. Diets yielding butyrate and acetate from bacterial fermentation show increased <a href="/facts/Regulatory_T_cell/1ECRAGMg">Treg</a> expression.<a class="footnote-ref" id="fnref:256" href="#fn:256">256</a> <a href="/facts/Regulatory_T_cell/1ECRAGMg">Treg</a> cells <a href="/facts/Downregulation_and_upregulation/6nRoa28r">downregulate</a> <a href="/facts/T_cell/5z6PQ9UN">effector T cells</a>, which in turn reduces the <a href="/facts/Inflammation/Ura86MIy">inflammatory response</a> in the gut.<a class="footnote-ref" id="fnref:257" href="#fn:257">257</a> Butyrate is an energy source for colon cells. butyrate-yielding diets thus decrease <a href="/facts/Intestinal_permeability/zQThl74p">gut permeability</a> by providing sufficient energy for the formation of <a href="/facts/Tight_junction/CXxxM5H5">tight junctions</a>.<a class="footnote-ref" id="fnref:258" href="#fn:258">258</a> Additionally, butyrate has also been shown to decrease insulin resistance, suggesting gut communities low in butyrate-producing microbes may increase chances of acquiring <a href="/facts/Diabetes_mellitus_type_2/zCMXksmt">diabetes mellitus type 2</a>.<a class="footnote-ref" id="fnref:259" href="#fn:259">259</a> Butyrate-yielding diets may also have potential <a href="/facts/Colorectal_cancer/nV592sW7">colorectal cancer</a> suppression effects.<a class="footnote-ref" id="fnref:260" href="#fn:260">260</a>

<h3>Obesity and metabolic syndrome</h3>
The gut flora have been implicated in obesity and <a href="/facts/Metabolic_syndrome/jI70tRBv">metabolic syndrome</a> due to a key role in the digestive process; the Western pattern diet appears to drive and maintain changes in the gut flora that in turn change how much energy is derived from food and how that energy is used.<a class="footnote-ref" id="fnref:261" href="#fn:261">261</a><a class="footnote-ref" id="fnref:262" href="#fn:262">262</a> One aspect of a <a href="/facts/Healthy_diet/sjJBXc4l">healthy diet</a> that is often lacking in the <a href="/facts/Western-pattern_diet/6fdL7lIc">Western-pattern diet</a> is fiber and other complex carbohydrates that a healthy gut flora require flourishing; changes to gut flora in response to a Western-pattern diet appear to increase the amount of energy generated by the gut flora which may contribute to obesity and metabolic syndrome.<a class="footnote-ref" id="fnref:263" href="#fn:263">263</a> There is also evidence that microbiota influence eating behaviours based on the preferences of the microbiota, which can lead to the host consuming more food eventually resulting in obesity. It has generally been observed that with higher gut microbiome diversity, the microbiota will spend energy and resources on competing with other microbiota and less on manipulating the host. The opposite is seen with lower gut microbiome diversity, and these microbiotas may work together to create host food cravings.<a class="footnote-ref" id="fnref:264" href="#fn:264">264</a>
Additionally, the liver plays a dominant role in <a href="/facts/Blood_glucose/I4SkNzrm">blood glucose</a> homeostasis by maintaining a balance between the uptake and storage of glucose through the metabolic pathways of <a href="/facts/Glycogenesis/W5oCLM4F">glycogenesis</a> and <a href="/facts/Gluconeogenesis/Jj5THIHh">gluconeogenesis</a>. Intestinal lipids regulate glucose homeostasis involving a gut–brain–liver axis. The direct administration of lipids into the upper intestine increases the long chain fatty <a href="/facts/Acyl-coenzyme_A/uWNxxzSj">acyl-coenzyme A</a> (LCFA-CoA) levels in the upper intestines and suppresses glucose production even under subdiaphragmatic <a href="/facts/Vagotomy/nvKkmMDW">vagotomy</a> or gut vagal <a href="/facts/Deafferentation/2KjA7nyD">deafferentation</a>. This interrupts the neural connection between the brain and the gut and blocks the upper intestinal lipids' ability to inhibit glucose production. The gut–brain–liver axis and gut microbiota composition can regulate the glucose homeostasis in the liver and provide potential therapeutic methods to treat obesity and diabetes.<a class="footnote-ref" id="fnref:265" href="#fn:265">265</a>
Just as gut flora can function in a feedback loop that can drive the development of obesity, there is evidence that restricting intake of calories (i.e., <a href="/facts/Dieting/KGzfTQrj">dieting</a>) can drive changes to the composition of the gut flora.<a class="footnote-ref" id="fnref:266" href="#fn:266">266</a>

<h2 id="other-animals">Other animals</h2>
The composition of the human gut microbiome is similar to that of the other great apes. However, humans' gut biota has decreased in diversity and changed in composition since our evolutionary split from Pan.<a class="footnote-ref" id="fnref:267" href="#fn:267">267</a> Humans display increases in Bacteroidetes, a bacterial phylum associated with diets high in animal protein and fat, and decreases in Methanobrevibacter and Fibrobacter, groups that ferment complex plant polysaccharides.<a class="footnote-ref" id="fnref:268" href="#fn:268">268</a> These changes are the result of the combined dietary, genetic, and cultural changes humans have undergone since evolutionary divergence from Pan.
In addition to humans and vertebrates, some insects also have complex and diverse gut microbiota that play key nutritional roles.<a class="footnote-ref" id="fnref:269" href="#fn:269">269</a> Microbial communities associated with <a href="/facts/Termite/KRFbDumW">termites</a> can constitute a majority of the weight of the individuals and perform important roles in the digestion of <a href="/facts/Lignocellulose/b9EkMneQ">lignocellulose</a> and <a href="/facts/Nitrogen_fixation/TeLoBpWS">nitrogen fixation</a>.<a class="footnote-ref" id="fnref:270" href="#fn:270">270</a> It is known that the disruption of gut microbiota of termites using agents like antibiotics<a class="footnote-ref" id="fnref:271" href="#fn:271">271</a> or <a href="/facts/Boric_acid/0so68XIK">boric acid</a><a class="footnote-ref" id="fnref:272" href="#fn:272">272</a> (a common agent used in preventative treatment) causes severe damage to digestive function and leads to the rise of opportunistic pathogens.<a class="footnote-ref" id="fnref:273" href="#fn:273">273</a> These communities are host-specific, and closely related insect species share comparable similarities in gut microbiota composition.<a class="footnote-ref" id="fnref:274" href="#fn:274">274</a><a class="footnote-ref" id="fnref:275" href="#fn:275">275</a> In <a href="/facts/Cockroach/mKJP7W6j">cockroaches</a>, gut microbiota have been shown to assemble in a deterministic fashion, irrespective of the <a href="/facts/Inoculation/M2LPGM66">inoculum</a>;<a class="footnote-ref" id="fnref:276" href="#fn:276">276</a> the reason for this host-specific assembly remains unclear. Bacterial communities associated with insects like termites and cockroaches are determined by a combination of forces, primarily diet, but there is some indication that host <a href="/facts/Phylogeny/f5vVEpeY">phylogeny</a> may also be playing a role in the selection of lineages.<a class="footnote-ref" id="fnref:277" href="#fn:277">277</a><a class="footnote-ref" id="fnref:278" href="#fn:278">278</a>
For more than 51 years it has been known that the administration of low doses of antibacterial agents promotes the growth of farm animals to increase weight gain.<a class="footnote-ref" id="fnref:279" href="#fn:279">279</a>
In a study carried out on <a href="/facts/Mice/6m1X7m0g">mice</a> the ratio of Firmicutes and <a href="/facts/Lachnospiraceae/KHTXaHAW">Lachnospiraceae</a> was significantly elevated in animals treated with subtherapeutic doses of different antibiotics. By analyzing the caloric content of faeces and the concentration of small chain fatty acids (SCFAs) in the GI tract, it was concluded that the changes in the composition of microbiota lead to an increased capacity to extract calories from otherwise indigestible constituents, and to an increased production of SCFAs. These findings provide evidence that antibiotics perturb not only the composition of the GI microbiome but also its metabolic capabilities, specifically with respect to SCFAs.<a class="footnote-ref" id="fnref:280" href="#fn:280">280</a>

<h2 id="see-also">See also</h2>
<ul>
<li>Biology portal</li><li>Medicine portal</li></ul>
<ul><li><a href="/facts/Colonisation_resistance/UdJtdYQ8">Colonisation resistance</a></li>
<li><a href="/facts/List_of_human_flora/KerK9YGP">List of human flora</a></li>
<li><a href="/facts/List_of_microbiota_species_of_the_lower_reproductive_tract_of_women/Vmph4v5H">List of microbiota species of the lower reproductive tract of women</a></li>
<li><a href="/facts/Skin_flora/jxUPFoB4">Skin flora</a></li>
<li><a href="/facts/Verotoxin-producing_Escherichia_coli/xhtWPSCd">Verotoxin-producing Escherichia coli</a></li></ul>
<h2 id="notes">Notes</h2>

<h2 id="further-reading">Further reading</h2>
Review articles
<ul><li>De Preter V, Hamer HM, Windey K, et al. (2011). "The impact of pre- and/or probiotics on human colonic metabolism: Does it affect human health?". Molecular Nutrition & Food Research. 55 (1): 46–57. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1002%2Fmnfr.201000451">10.1002/mnfr.201000451</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/21207512">21207512</a>.</li>
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</ol>

Gut microbiota open-in-new

Gut microbiota