Skin Microbiome Test

The gut microbiome is our second immune system. It also plays a fundamental role training our body’s immune system. A person with a healthy gut, this partnership between the immune system & the microbiota helps build protective responses to pathogens. An imbalanced microbiome has been observed to lead to autoimmune and inflammatory disorders. Moreover it is now been established that the lack of diversity also increases chance of infection not only in the gut but others parts of the body as well.

The team that developed BugSpeaks recently published an article in Virus Research which showed the potential connection between the gut microbiome and infectious lung diseases. The link to the article is shared under Related Publications.

It has long been recognized that the gut microbes contribute to the vitamins needs of our body. The magnitude of this contribution in healthy individuals is immense. In the state of an imbalanced gut, this contribution is decreases. Thiamine, folate, biotin, riboflavin, and panthothenic acid are available through diet and is also synthesised by the gut flora. It has been estimated that half of the body’s daily Vitamin K requirements comes from the gut microbiota.

The other interesting facet of bacteria synthesised vitamins are that their molecular structure is not identical to dietary vitamins. There are also specialized transporters that is synthesised by our body to distribute these vitamins. In all, this suggests that gut flora synthesised vitamins might have specific functions and are essential for health.

Gut microbiome plays a crucial role in the bi-directional communication between the gut and the brain. Recent research suggests that the gut microbiota can influence brain function via both the neuroimmune pathway and neuroendocrine pathways.

Studies have shown that microbial diversity and taxonomic compositions were significantly changed in people with mood disorders as compared to healthy individuals. Most of the research studies revealed that short-chain fatty acids-producing bacterial genera were decreased, while pro-inflammatory genera and those involved in lipid metabolism were increased in patients with depressive episodes.

High weight and normal weight individuals have a differential composition of their microbiome. Mechanistic studies have indicated that the microbiota can influence both sides of the energy balance equation; namely, as a factor influencing energy utilization from the diet and as a factor that influences host genes that regulate energy expenditure and storage. Recent studies on overweight adults showed that the ratio of bacteria in the gut co-related with weight loss. Those with higher ratios for particular set of bacteria lost more weight and body fat after 6 months than individuals with a low ratio, despite being on the same diet.

It is now clear that weight loss is more depended on what microbes are present in the gut than what food is actually consumed.

The mother's microbiome is known to influence, everything from hormonal changes to metabolic changes during pregnancy to even obstetrical syndromes. In a recent trial supplementation of probiotics combined with dietary counselling have found to improve gestational diabetes in pregnant women. In another study a good healthy gut microbiome was reported to reduce blood pressure in pregnancy as well as the incidence of preeclampsia among primiparous women

Composition of the mother’s gut microbiome, significantly influence the pregnancy, along with reduced risk of obstetrical syndromes, and a better health status of the newborn. The Maternal Microbiome sets the tone of Neonatal Microbiome, and it sets in at the time of birth.

The relationship between the microbiota and blood pressure is a complex one. Researchers have identified multiple possible hypotheses to link dysbiosis and hypertension. In Hypertension, the number of “good bacteria” decreased and the number of “bad bacteria” in the gut increased. Studies have also shown that transplant of microbial content from donor hypertensive animals can reproduce hypertension in previously normal (non-hypertension) recipient animals.

Studies have clearly identified that a bad microbiome can cause hypertension and also can progressively worsen hypertension.

Trimethylamine-N-oxide (TMAO) is a product of microbial-human co-metabolic pathway, which is derived from dietary (food based) choline and carnitine and converted to trimethylamine (TMA) by anaerobic bacteria residing within the lumen of the gut. TMA is then oxidized by a liver enzyme to TMAO. This TMAO is known to be a pro-atherogenic compound, which is directly implicated in the development of plaques inside the arteries. A dysbiosis in the intestinal microbiota, resulting in increased anaerobic bacteria, is thought to contribute to the chronic inflammatory state, production of TMAO and eventually atherosclerosis.

Parkinson’s disease (PD) is a whole body disease clinically defined by the degeneration of nerves in the brain, leading to symptoms like stiff muscles, difficulty with bodily movements, tremors, sleep issues, difficulty speaking, anxiety or apathy and much more. Other than the genetic factors, the role and the contribution of various environmental and lifestyle factors have gained importance recently. Importantly, about 60% of the PD patients suffer from constipation and other gut related issues from up to 20 years before the diagnosis of Parkinson’s. Hence, alterations in the gut microbiome composition have been studied, reported and their functional consequences have been associated with gut-brain axis and Parkinson’s.

The human gut microbiota and their metabolites can regulate immune cells and cytokines via epigenetic modifications. For example, short-chain fatty acids (SCFAs) produced by gut microbiota promote the differentiation of natural T cell into Treg cells by suppressing histone deacetylases (HDACs). Thus, resulting bacterial metabolites cause aberrant immune responses via epigenetic modifications, leading to Rheumatoid arthritis.

Delivery of undigested protein to the colon results in the proliferation of proteolytic bacteria. These bacteria ferment proteins and amino acids to generate potential uremic toxins, including p-cresol, indoxyl sulfate and trimethylamine N-oxide. Impaired gut barrier function allows translocation of uremic toxin into systemic circulation. This contributes to chronic kidney disease (CKD) progression.

Microbiota promote the absorption of monosaccharides from the gut, thereby triggering lipogenesis in the liver. Dysbiosis is associated with reduced synthesis and secretion of fasting-induced adipocyte factor a powerful metabolism and adiposity regulator belonging to the angiopoietin-like protein family in enterocytes, which results in increased activity of lipoprotein lipase (LPL), responsible for the secretion of triglycerides (TG) from very low-density lipoprotein, eventually resulting in the augmented uptake of fatty acids and accumulation of TG in the adipocytes and leading to NAFLD.

There are two important luminal (gut) factors, modulated by the gut microbiota, which maintains smooth muscle contraction and balanced bowel movements. The factors include short chain fatty acids (SCFAs) and bile acids. The absence of SCFAs due to low-fiber diet inhibit mucin secretion by intestinal goblet cells, reduce stool volume by stimulating water and electrolyte absorption, and inhibit smooth muscle contraction in the colon, causing imbalanced bowel movements/constipation.

A dysbiotic microbiota can result in the loss of colonization resistance due to changes in the structural and/or metabolic environment. The loss of specific community members potentially affects the levels of microbial and host-generated metabolites, resulting in a different functional state that promotes spore germination and vegetative outgrowth. A dysbiotic microbiota may also result in an imbalanced immune response through the loss of immune regulation and a proinflammatory state, both of which may affect disease development. Toxin production by vegetative C. difficile can stimulate the production of inflammatory cytokines, neutrophils, and antitoxin antibodies.

Gut bacteria like Escherichia coli, Bacteroides fragilis Enterococcus etc., produces toxins that are reported to be involved in the development of cancers. Specifically, these toxins are called enterotoxigenic (in simpler terms - toxic to genes), which means these toxins can directly damage the DNA resulting in activation of uncontrollable cell proliferation, which eventually leads to cancer.

Increased abundance of Enterobacteriaceae activates other enteric pathogens that trigger a set of inflammatory pathways, causing irritation of your gut. For instance, Sulfate reducing bacteria inflame the lining of the gut, while Clostridium and certain fungi trigger the factors that decrease anti-inflammatory bacteria (Lactobacillus, Faecalibacterium), cumulatively triggering or inducing to Crohn's disease.

The abundant bacteria in the gut needs complex polysaccharides to survive, which if absent in your gut, starts eating the mucus layer shielding the colon lining which leads to many opportunistic infections aided by Roseburia and Actinobacteria, which will further activate several enteric pathogens and triggers inflammatory pathways and causes inflammation in walls of gastrointestinal tract.

The gut microbiota is important in the development and regulation of intestinal immunity. The intestinal immune system interacts with the gut microbiota and helps in maintaining normal gastrointestinal functions, and any alteration in gut microbiota may be associated with activation of mucosal immunity and cause inflammation. Intestinal infection with pathogenic bacteria results in a transient disruption of the resident gut microbiota which is a risk factor for IBS. Release of these inflammatory mediators are known to cause irritable bowel syndrome.