Gut health and chronic disease prevention -
The PBAC classes, families, and genera differ in motion and metabolic activities. They have different shapes. Some have flagella, some are non-motile, while some perform bacteria gliding [ 34 , 35 ]. The PBAC is facultative or obligatory anaerobic. They can be chemoautotrophs or heterotrophic, and they are pathogens [ 34 , 35 ].
Some classes and genera are of considerable importance to medical experts, food industries, and scientists within this phylum. Class Gammaproteobacteria includes important pathogens, Salmonella , Vibrio , Pseudomonas , Escherichia , and Yersinia.
Genera such as Helicobacter and Campylobacter from class Epsilonproteobacteria are common in the GIT [ 34 ]. Proteobacteria are allied to inflammation; therefore, their population increases in the gut in a condition prone to inflammation [ 31 , 36 ].
Proteobacteria are called purple bacteria because of reddish pigmentation [ 32 ]. Actinobacteria ABAC , another populous bacteria in the human gut, are gram-negative bacteria and are mainly aerobic, even though some can survive under anaerobic conditions [ 37 , 38 ].
The ABAC has other characteristics; The DNA of ABAC contains a high level of Guanine and Cytosine [ 37 ]. Even though there are several genera, the pathogens that live in humans include Mycobacterium, Corynebacterium, Nocardia, and some species of Streptomyces [ 37 , 38 ].
The ABAC are secondary producers of metabolites; therefore, they are of interest for pharmacological and commercial purposes. The subclass Actinobacteridae and the order Actinomycetales are particularly of medical and economic benefit because their metabolites have antibiotics, particularly the genus Streptomyces [ 37 , 38 ] Figure 3.
Mycobacterium tuberculosis , one of the species of Actinobacteria hosted by humans [ 39 ]. Firmicutes are gram-positive bacteria, though some have a pseudo outer membrane that makes them stain gram-negative [ 35 , 40 ].
Phylum Firmicutes is notable for microorganisms that profer health benefits. Some genera of Firmicutes are administered as probiotics to profer gut health benefits. Characteristics include; Firmicutes could be round cocci or rod-like bacillus in shape. Unlike the ABAC, they have a low level of Guanine and Cytosine in their DNA; they are acid-tolerant and take part in metabolic and physiological activities [ 35 , 40 ].
There are two major classes; the anaerobic Clostridia and the obligate or facultative aerobic Bacilli [ 35 , 40 ]. These are notable pathogens and beneficial microorganisms within this phylum.
One crucial order of this phylum is the Lactobacillales Lactic Acid Bacteria. Lactic acid bacteria produce lactic acid as a metabolite during glucose fermentation. Lactic Acid Bacteria appear everywhere in the food and are therefore regarded safe for consumption.
In addition, they are known to contribute health benefits to the human gut [ 35 , 40 ]. The genera for Lactic Acid Bacteria include Lactococcus , Enterococcus , and Streptococcus. The genus Lactobacillus Figure 4 is the most common microbe used as probiotics [ 35 , 40 ]. Firmicutes are either anaerobic, particularly Clostridia , while class Bacilli is an obligate or facultative aerobe.
Therefore, bacteria belonging to class Bacilli would not grow or populate in an anaerobic environment [ 35 , 40 ]. Lactobacillus paracasei [ 41 ].
Bacteroidetes are gram-negative, non-spore-forming, and anaerobic bacteria [ 42 ]. Bacteroidetes can survive in several environments, including the gut and skin. The class Bacteroidia is the most studied class of this phylum GM [ 42 ].
One common genus in this class is the Bacteroides. Bacteroides are clinically significant and have a mutualistic relationship with the host [ 42 , 43 ]. The mutualistic behavior of Bacteroides occurs if they are retained in the gut.
Once Bacteroides escape their familiar environment, they become pathogenic and can cause diseases such as an abscess in different parts of the body [ 43 ]. Other features of Bacteroides include: Bacteroides break down large molecules in the human guts into simpler molecules, while the bacteria derive their energy source from their host.
The bacteria hence help to produce beneficial fatty acids [ 42 , 43 ]. Bacteroides prevent other pathogens from colonizing and infecting the gut of the host [ 42 ]. Bacteroides have species that are highly resistant to many antibiotics [ 43 ]. The GM is a balanced environment of different microorganisms such as bacteria, viruses, bacteriophages, archaea, and fungi; however, the bacteria community preserves the homeostasis of the gut.
The bacteria community contains some groups of gut bacteria that produce SCFAs mentioned in Section 2. These fatty acids include acetate, propionate, and butyrate. The SCFAs are an essential fuel for the intestinal epithelial cells, and they assist the gut barrier functions and sustain homeostasis in the intestine [ 23 , 44 ].
These groups of gut bacteria ferment indigestible dietary fibers to produce SCFAs. Dietary fibers such as resistant starch, inulin, wheat, oat bran, cellulose, pectin, and Guam gum are suitable substrates for bacteria activities and fermentation.
Out of all prominent bacteria phylum identified in the human body, the Firmicutes and Bacteroidetes are more of the SCFAs producers [ 23 , 44 ]. The acetate and propionate are produced by phylum Bacteroidetes, while the Firmicutes produce more of the butyrate [ 23 , 45 ].
Another genus, such as Bifidobacterium , from phylum Actinobacteria and some Proteobacteria, could also produce butyrate.
It is also important to note that some butyrate producers like Bacteroides are anaerobic bacteria and would not be active in aerobic situations; however, class Bacilli of Firmicutes would thrive because they are aerobes [ 23 , 35 , 46 ].
The aerobic environment in a human gut will suppress the growth of some butyrate-producing bacteria but allow the growth of aerobic pathogens like Salmonella typhimurium [ 23 ]. The SCFAs control the gene expression for energy metabolism.
Butyrate, in particular, is the primary energy source for colon cells. Therefore, SCFAs are involved in the energy metabolism of colon epithelial cells [ 23 , 47 , 48 ].
Propionate act as gluconeogenesis substrate in the intestine, where it can be oxidized to glucose. Acetate is also available in the tissues, where it can be transformed to butyrate and oxidized by muscles or used for lipogenesis [ 27 , 49 ].
The SCFAs regulate the development of organoids. Hence, a cell proliferating attribute. The SCFA can induce mucus-secreting cells to secrete mucus that protects the mucosa [ 23 , 48 ]. The SCFAs have been identified to suppress cancer cells or causing apoptosis to cancer cells.
In addition, they perform the antimicrobial function because they can disrupt the osmotic and pH balance, creating an environment not accommodative to other microorganisms [ 48 ].
The SCFAs promote epithelial barrier function by initiating genes responsible for tight junctions and reforming protein, increasing epithelial resistance to pathogen invasion [ 23 , 48 ]. The SCFAs induce prostaglandins which have an anti-inflammatory effect, thus reducing the pro-inflammatory effect.
The colonization of GM starts from childbirth; however, the composition starts changing based on different factors. For example, researchers reported that the type of bacteria composition in children fed with breast milk differs from children fed with the formula [ 14 , 22 ].
In the same way, children born via natural birth have different GM compositions from children born via assisted delivery, such as caesarian surgery [ 14 , 22 ]. As infants are introduced to solid food, GM composition makes another change [ 14 , 22 ].
It is also important to note that the composition of GM also differs based on the part of GIT. For instance, the types of GM in the colon are different from the types in the stomach. This difference is because of factors such as the redox condition of the different organs.
Other factors are the pH of the organ environment, allergies, the motility of organs, secretions in each organ such as the gastric acid secretion of the stomach, and the undamaged ileocaecal valve [ 14 , 22 ]. Bacteria colonizing the guts from birth are also referred to as commensal bacteria because they benefit the host [ 14 , 51 ].
For instance, Bacteroidetes and Firmicutes are the major phyla involved in breaking down macromolecules into simpler forms, particularly the indigestible fibers.
However, abnormal changes can occur to the GM, leading to an abnormal composition of bacteria. This condition can be the onset of chronic diseases such as type 1 and 2 diabetes, obesity, cardiovascular diseases, cancer, and inflammatory bowel diseases [ 14 , 52 ].
Surprisingly, abnormal bacteria composition has been linked with diseases that are considered temporary due to physiological changes like metabolic and immunological changes [ 7 , 53 ].
An example is a gestational diabetes. During pregnancy, some women who cannot produce enough insulin develop gestational diabetes.
The physiological changes occurring during pregnancy, such as weight gain, reduce the effective use of insulin, resulting in insulin resistance, as shown in Figure 5. The development of insulin resistance makes the body of the pregnant woman demands more insulin production.
Even though gestational diabetes occurs late in pregnancy, some women experience insulin resistance before pregnancy [ 53 , 55 ]. Women with gestational diabetes, if not well managed, might have their unborn babies at risk of being over 9lbs weight birth, which could bring delivery hazards to the mother.
Also, the baby might be born earlier than anticipated, which could cause health problems for the baby. In addition, the baby might be born with low blood sugar. Changes in the GM population are noticed in people who have gestational diabetes and chronic diseases.
This change in population is the gut dysbiosis. Insulin resistance during gestational diabetes [ 54 ]. Gut dysbiosis is a condition in which there is a change in the balance of GM composition. Some phyla become highly populated while some reduce in population. This condition creates abnormality in the human GIT, and the pathogenesis of commensals bacteria starts [ 52 ].
Most bacteria in the gut are beneficial; however, when the balance in population changes in these bacteria gut colonies, as shown in Figure 6 , dysbiosis occurs [ 7 , 52 ]. Some symptoms of dysbiosis are mild and temporary; however, leaving dysbiosis untreated could result in severe symptoms associated with chronic diseases [ 52 ].
Even though commensals bacteria antagonize invading microorganisms, sometimes foreign microorganisms can seize the epithelium and overthrow the commensals, destabilizing the immune response [ 52 ]. After that, the invading pathogens induce inflammation to which they would be resistant, facilitating their growth and changing the balance of commensals bacteria.
Viruses create series of mechanisms that regulate the activities of the commensals, making them harmful to the host [ 16 , 58 ]. Factors causing dysbiosis include a dietary change, chemical consumption like insecticides, alcoholism, improper use of medications, particularly antibiotics, poor dental hygiene, unprotected sex, stress, and anxiety, psychological stress.
All these factors could change the balance of GM. In addition, the genotype and immune metabolic functions can alter the population of commensal microbes [ 52 , 59 , 60 ].
Gut dysbiosis [ 57 ]. Symptoms of dysbiosis are dependent on the location of GM imbalance development and the types of bacteria involved. Symptoms could be gas, bloating, diarrhea, constipation, and cramps [ 52 , 61 ]. To determine the imbalance of GM, most researchers make use of a human stool [ 52 , 62 ].
The organic acid test is another test used medically to determine imbalance [ 52 , 62 ]. Some bacteria produce organic acids as metabolites. The hydrogen breath test is another test conducted to determine dysbiosis.
In this case, gases from the mouth are tested for imbalance [ 52 , 62 ]. Unfortunately, diseases tolerance varies in people; not everyone with dysbiosis shows severe symptoms that call for urgent attention or medical checkup, particularly at a young age.
Ignoring or leaving the dysbiosis untreated, however, can result in many severe diseases. The GM is partly responsible for the physiology of the body systems. Changes in the balance or population of GM have been linked to bowel diseases, allergies, and chronic metabolic diseases such as diabetes, obesity, cardiovascular diseases, and short-term disease like gestational diabetes.
According to research, Firmicutes such as Lactobacillus , Actinobacteria such as Bifidobacterium decreased in populations in children diagnosed with type 1 diabetes. In contrast, the population of Firmicutes such as Clostridium and Veillonella , Bacteroidetes like Bacteroides and Prevotella increased [ 14 , 15 ].
Patients with Type 1 diabetes had low butyrate-producing and mucin degrading microbes, while pathogenic bacteria increased in population in the gut. Butyrate-producing bacteria and mucin degrading microbes are good for gut health [ 14 , 63 ]. The functions of SCFAs, of which butyrate is one, are discussed in Section 4.
Mucin degradation releases complex carbohydrates and produces SCFAs like acetate and propionate [ 64 ]. In patients with type 2 diabetes, Clostridia and Bacilli Firmicutes decreased in population while PBAC increased. Butyrate-producing microorganisms like Firmicutes are known to produce SCFAs. The increase in blood glucose is because the host will seek the missing calories by consuming more food.
Lack or low butyrate concentration could also reduce satiety, making the host eat more, thus raising blood glucose [ 30 , 47 , 66 ]. Proteobacteria, which are more dominant in type 2 diabetes, induce inflammatory responses [ 36 , 47 ].
An alteration in PBAC composition is common in metabolic syndromes causing diseases. In a study where the fecal samples of patients with type 2 diabetes were analyzed, a significant number of Enterobacteriaceae, a family from the phylum PBAC, were found [ 14 , 31 ].
At the initiation of an inflammatory response, specific proteins are released into the bloodstream. These proteins inhibit insulin secretion and build insulin resistance in the body [ 14 , 67 ].
The profile of GM in women with gestational diabetes is similar to patients who have type 2 diabetes [ 53 , 68 ]. In a study to determine the onset of dysbiosis in pregnant women, GM was typical in pregnant women in their first semester trimester.
However, by the third trimester, the population of Proteobacteria and Actinobacteria increased while butyrate-producing microorganisms like Faecalibacterium and Eubacterium from phylum Firmicutes reduced. In addition, the Enterobacteriaceae family and Streptococcus were also numerous.
Even though scientists observed Bacteroidetes and Firmicutes throughout all three trimesters of the pregnancy [ 68 , 69 ]; however, the strong negative relationship between Bacteroidetes and Firmicutes phyla in healthy pregnant women was missing in women with gestational diabetes [ 7 ].
Most of the GM reduced were SCFA producing bacteria. The absence of these bacteria in pregnant women reduced the physiological function of the intestine.
The gut permeability was not regulated, insulin sensitivity was reduced, inflammatory response that can lessen the development of diabetes was equally reduced [ 7 ].
Gut dysbiosis could be a biomarker for gestational diabetes, and a test of dysbiosis could be early detection before the pregnancy reaches the third trimester [ 7 ].
Changes in the GM population was associated with diet and weight gain during pregnancy [ 53 , 68 ]. Bacteria belonging to Firmicutes and Actinobacteria were decreased, some of which had a probiotic effect, while PBAC and Ruminococcus gnavus , another Firmicutes associated with inflammation, were increased [ 14 , 24 , 31 , 70 ].
The PBAC is signaled as a pointer to instability in the microbiota. Therefore, an increase in the PBA C population is found in people with IBD disease. Even though the exact reason for the increase in PBAC is unknown, it is hypothesized that PBAC, with its inflammatory effect, creates anaerobic conditions in the gut.
The beta-oxidation process reduces when proinflammation occurs. Therefore, anaerobic conditions contribute to the growth of PBAC, which are facultative anaerobe, thereby allowing dysbiosis [ 14 , 15 ].
Anaerobic conditions increase the growth of pathogenic Firmicutes but reduce the population of the beneficial Firmicutes, like the Lactic Acid Bacteria [ 35 , 40 ]. Another IBD due to dysbiosis is ulcerative colitis [ 14 , 15 ].
Scientists discovered that Lactobacilli were low in composition in patients with ulcerative colitis at an active stage, while the Clostridiales order of Firmicutes was more prominent. High Escherichia coli was equally identified in people with active ulcerative colitis.
Inflammation seen in IBD is associated with the decreased colonization resistance [ 14 , 15 ]. Inflammatory Bowel Diseases IBD occur when genetic and environmental factors encourage the growth of pathogens that can decrease the population of commensals, thereby causing inflammation [ 15 ].
In addition, IBD can occur when there is an unusual immune response against commensal bacteria. For example, sometimes immune cells such as macrophages could not recognize GM and trigger an immune response which attacks the intestinal wall [ 15 ].
Hence, Firmicutes and Bacteroidetes decrease while PBAC increases. When the GM composition of healthy and patients with obesity were compared, anaerobic Firmicutes and Proteobacteria were increased in the fecal samples of patients.
At the same time, Bacteroidetes decreased compared to a healthy individual. The high ratio of Firmicutes and Bacteroidetes has been linked to obesity [ 14 , 71 ].
A significant increase in Enterobacteriaceae, PBAC family, was equally found in patients with obesity. This population of PBAC family reduced after the patient lost weight [ 31 ]. In a study on mice, a toll-like receptor 5, a sensor that detects microbial infection to initiate an immune response, was deficient when fed with a high-fat diet.
The masking of toll-like receptor 5 concealed the changes occurring in the GM, and the body could not produce an immune response to fight the strange invading organisms [ 51 , 72 ]. Deficiency of this receptor has been linked to hypertension, insulin resistance, and weight gain, though the exact reason for the masking was uncertain [ 15 , 73 ].
Microbiota dysbiosis was related to the development of cardiovascular diseases. A high level of PBAC was found in arteriosclerosis plaque, indicating PBAC has the pro-inflammatory effect that can cause plaque [ 15 , 74 ].
In addition, some scientists reported that GM converts choline, an essential body nutrient, to trimethylamine, an organic compound. Trimethylamine is further processed in the liver to trimethylamine N-oxide which is known to increase arterial plaques.
An increase in arterial plaque can cause arteriosclerosis diseases [ 14 , 15 ]. In another study, Gammaproteobacteria, a class of PBAC, was connected with endogenous alcohol production linked to the cause of non-alcoholic fatty liver diseases, which is associated with increased risk of cardiovascular failure incidence [ 75 ].
Inflammation caused by some phylum of GM could create a grave environment for the development and growth of cancer cells. Even though cancer linked to microbiota so far occurs in body parts that house the GM, notably the GIT, the colon [ 15 , 76 ].
Commensals sometimes take up pathogenic features when invaded, giving them pathogenic effects; such commensals are called pathobionts. In a study on mice, pathobionts and pathogens contributed to the uncontrolled epithelial cell growth of the colorectal region [ 15 ].
Some scientists also suggested that some GM like Bacillus fragilis , a Bacteroidetes are virulent and can modify the GM to favor inflammatory responses. These inflammatory responses could cause alterations in the epithelial cells, and this could result in cancer. In addition, people with chronic inflammatory disarray have been discovered to have a high susceptibility to gastric cancer and cancer of the lymphatic system associated with the mucosa [ 76 ].
Research continues on how GM and its activities cause chronic diseases. From completed studies, it is apparent that the composition of the gut differs between diseased and healthy individuals.
While a significant population of commensals and SCFAs producing bacteria reduced, the pathogenic population increased and influenced the commensals, making them turn against the host.
Pathogens equally created unfavorable conditions such as inflammatory or anaerobic conditions. The change in the environment favored the growth of pathogens but reduced the growth of commensals. To take care of gut health, the types of food consumed determines the type of GM. Butyrate maintains colonic homeostasis and prevents inflammation, and maintains mucosal integrity [ 44 ], thereby playing a role in reducing dysbiosis.
Therefore, food rich in these fermentable dietary fibers would be suitable for gut health [ 25 , 44 ]. The types of protein consumed matter to gut health. Animal protein fermentation decreases the production of SCFAs, increasing the risk of IBD [ 25 ].
However, consuming plant-based protein is associated with an increase in beneficial GM like Bifidobacterium , Lactobacillus, and it increases the production of SCFA [ 25 , 44 ]. High consumption of polyunsaturated fatty acids has been associated with an increased healthy GM population like Lactobacillus and Roseburia , thus increasing the production of SCFA-butyrate [ 25 , 44 ].
In contrast, high consumption of sodium and food additives such as sweeteners are associated with changes in the composition of GM. When food is high in sodium, it reduces the population of commensal microorganisms like Lactobacillus. Also, food additives cause a significant change in the population of the balanced gut system [ 25 , 44 ].
What humans eat can determine gut health, and the composition of GM in the gut contributes to overall well-being. Asides healthy diet, there are other ways to improve gut health. One of these ways is the use of probiotics as supplements. Probiotics are live microorganisms made into pills that profer health benefits when administered in adequate amounts.
In addition, the use of prebiotics has equally been suggested. Prebiotics are not microorganisms but non-digestible substances that benefit the host by improving the growth and activities of selected bacteria in the gut [ 77 , 78 , 79 ].
Other methods are requiring medical experts and scientists. One is fecal microbiota transplantation, which involves infusing stool from a healthy donor to a recipient by delivering the stool through the upper GIT [ 80 ].
This method requires adequate care to ensure the feces transferred to other patients do not have infectious microorganisms. Other methods being used include phage therapy, bacteria consortium transplantation, and the use of predatory bacteria [ 81 ].
Special thanks to Olukayode Olubowale and Oluwaseun Sanusi for their contribution to the content of the chapter. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Edited by Miroslav Radenkovic. Open access peer-reviewed chapter The Interaction between the Gut Microbiota and Chronic Diseases Written By Temitope Sanusi-Olubowale.
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Chapter metrics overview Chapter Downloads View Full Metrics. Impact of this chapter. Abstract The world is experiencing an increase in chronic diseases like diabetes, inflammatory bowel diseases, cancer, cardiovascular diseases, obesity, and diabetes preceding disease like gestational diabetes.
Keywords Gut microbiota Bacteria phylum Gestational diabetes Chronic diseases Gut dysbiosis. Introduction Chronic diseases CD are unfavorable health statuses lasting for over one year or more [ 1 , 2 ].
References 1. Centers for Disease Control and Prevention. About Chronic Diseases [Internet]. htm [Accessed: ] 2. Stoppler MC [Internet]. Medical Definition of Chronic disease. htm [Accessed: ] 3. World Health Organization. Integrated chronic disease prevention and control [Internet].
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Telford RD. Low physical activity and obesity: Causes of chronic disease or simply predictors? Thursby E, Juge N. Introduction to the Human Gut Microbiota.
Biochemical Journal. Zhang YJ, Li S, Gan RY, Zhou T, Xu DP, Li HB. Impacts of gut bacteria on human health and diseases. This interwoven relationship and constant communication between the gut microbiome and the immune system is the primary reason researchers search for cures to all sorts of illnesses by focusing on the gut.
This process has been implicated in:. This list is far from exhaustive. You can dive deeper into which diseases are linked to gut dysbiosis here. The gut microbiome acts as a conductor for the symphony, making sure everything plays in tune and on time. When your gut microbiome is out of harmony, it can throw off your hormones and cause a variety of health issues ranging from weight gain to thyroid dysfunction.
How Your Gut Microbiome Affects Your Mental Health. The gut-brain connection is constant and even has its designated line of communication—the vagus nerve. Changes in the gut microbiome are linked to the mind on many levels including: [14,15]. The gut-brain connection is so strong that one of the fastest growing areas of neuroscience looks at the gut first.
Beauty truly comes from the inside out. The gut microbiome plays a direct role in the appearance of your skin through influencing:. When it comes to autoimmune skin conditions such as eczema, rosacea, and psoriasis, the gut is known to be a major driver behind the worsening of these conditions.
You can read more about that here. Could the gut microbiome be a predictor of heart disease? Researchers from the University of Cambridge seem to think so. They found that specific metabolites, such as trimethylamine N-oxide TMAO , could be a good indicator of heart disease risk.
High levels of TMAO in the body occur when bacteria convert choline into trimethylamine TMA , which is then absorbed by the body and converted to the harmful version, TMAO.
Choline one of the B-complex vitamins is found in many animal products and legumes, which might make you want to cut back on these foods. However, the initial part of this conversion — from choline to TMA — only occurs when you have certain bacteria in your microbiome.
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Open access peer-reviewed Gut health and chronic disease prevention. Submitted: 20 Yealth Reviewed: 27 July Gur 23 August com customercare cbspd. The world is experiencing an increase in chronic diseases like diabetes, inflammatory bowel diseases, cancer, cardiovascular diseases, obesity, and diabetes preceding disease like gestational diabetes. Most of these diseases can be prevented and mitigated if individuals pay attention to the causative factors.
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