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is usually found in the mouth, playing a role in various diseases such as periodontitis, appendicitis, gingivitis and invasive infections in the other organs. Studies showed that F. nucleatum exerts the cancer pathogenesis through the interaction of three biomolecules located on the surface of the microbe: lipopolysaccharide (LPS), adhesin A (FadA), and fusobacterium autotransporter protein 2 (Fap2) [234]. Fiber‐enriched and low‐fat diet can reduce the risk of F. nucleatum‐positive colorectal cancer through the displacement of the pathogen from the gut; however, the dietary change does not show any significant improvements in F. nucleatum‐negative cancer patients [235]. These studies suggest the role of diet pattern in displacing F. nucleatum, thus negating the risk of colorectal cancer development, showing the relationship between diet, microbiome, and cancer pathogenesis.

      1.3.4 Psychological Disease

      Increasing studies on the brain–gut–microbiome (BGM) axis describe the bidirectional interactions between the central nervous system, gastrointestinal tract, and gut microbiota [236, 237]. Increasing evidence has proposed that this axis contributes largely to pathologies of some psychological diseases, such as autism spectrum disorder (ASD) [237, 238], Parkinson's disease (PD), and Alzheimer's disease (AD) [239, 240]. This section will discuss the dietary effects on ASD and neurodegenerative diseases.

      1.3.4.1 Autism Spectrum Disorder

      1.3.4.2 Neurodegenerative Diseases

      Neurodegenerative diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD) were found to be exacerbated by the disruption in gut microbiota, contributing to the pathogenesis of neurodegenerative disorders via the BGM [239, 257]. PD patients were reported to observe an increase in genus Lactobacillus, Bifidobacterium, and Akkermansia (pro‐inflammatory, mucin‐degrading Gram‐negative bacteria) population, and a decrease in the Faecalibacterium, Coprococcus, Blautia, Prevotella, and other microbes of the Prevotellaceae family (the bacteria responsible to SCFA production) [258, 259]. Dietary supplementation of specific probiotics, such as Lactobacillus and Bifidobacterium, was found to treat neurodegenerative symptoms in clinical trials and mice [260–262]. Phytochemicals, such as caffeine from ingested coffee and tea, were found to have an inverse relation, lowering the risk of developing PD. [263] It was also shown that caffeine confers neuroprotective properties in PD‐induced mice models [264, 265]. Similar to ASD, a ketogenic diet was identified to improve symptoms of PD and AD both in animal models and clinical trials [266–270]. These results indicate the role of diet in regulating the microbiota population involved in preventing neurodegenerative disease.

      1.3.5 Metabolic Disorder

      Metabolic disorders are caused by the dysbiosis of intestinal microbiota, resulting in changes in the host's ability to digest certain types of foods. This leads to various disease metabolic disorders such as obesity, diabetes, and non‐alcoholic fatty liver disease (NAFLD). In this chapter, we will discuss these metabolic disorders and their link to diet and the microbiome.

      1.3.5.1 Obesity

      The role of gut microbes in regulating fat storage in their human host is mainly attributed to the ability of these microbes to ferment complex polysaccharides that the host generally cannot absorb from the diet [273]. Microbes such as B. thetaiotaomicron have been shown to induce the expression of monosaccharide transporters in mice [274], where the polysaccharides are hydrolyzed into monosaccharides and SCFAs for easy absorption by the host intestinal cells. The increase of sugar uptake is then converted to lipids in the liver, triggering intestinal microbes to facilitate host expression fat metabolism gene Fiaf resulting in the accumulation of excessive fat [275]. Other studies have shown that orally introduced probiotics in mice fed with a high‐fat diet prevent the perturbation of intestinal mucosal permeability and limit energy absorption. These oral probiotics exert such bioactivity by reducing plasma LPS and cytokines and promote the gut secretion of glucagon‐like peptide‐1 (GLP‐1) and glucagon‐like peptide‐2 (GLP‐2) involved in maintaining the intestinal mucosal barrier [276].

      1.3.5.2 Diabetes

      Diabetes is a metabolic disorder that results in an increased sugar serum level, often resulting from the deficiency of insulin secretion or insulin insensitivity. Studies have shown that bacterial abundance in the gut has a strong correlation to the onset of diabetes. This has been shown in type II diabetes (T2D) patients that showed increased Firmicutes abundances with a proportional decrease in Bacteroidetes abundance. Long‐term observation of T2D patients undergoing weight loss showed a recovery of Bacteroidetes abundance and depletion of Firmicutes population [131]. It was discovered that the ratio of GI Firmicutes/Bacteroides affects the body metabolism, where patients with higher ratio were shown to be more susceptible to inflammatory responses, increased BMI, and a higher risk of developing insulin resistance that may lead to type 2 diabetes [271, 275, 277]. Certain studies indicated that orally administered prebiotics helps lower the ratio in hyperphagic, obese, and hyperglycemic mice model (ob/ob), which caused an increase in the number of L‐cells [278]. The increase of L‐cells raises the plasma levels of GLP‐1, triggering glucagon expression, resulting in leaner mice compared to the untreated groups.

      1.3.5.3

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