Till the 1990s, it has been a mystery as to whether the microbes/genes in the gut microbiome have any impact on human health other than the canonical role of the gut bacteria to break down food remnants, modulate the immune system, promote fat storage, biosynthesis of vitamins and amino acids, metabolism of drugs etc. But, with the advent of next generation sequencing and other genome enabled technologies including DNA based databases and metabolomics on human microbiome studies have become an eye-opener to hitherto unknown facts about the composition of gut microbiomes, their dynamics and their relevance to human welfare [
5]. At the phylum level
Bacteroidetes and
Firmicutes are the most dominant bacteria in the gut of normal individuals and together constitute 70–90% of the total bacterial community followed by
Actinobacteria and
Proteobacteria. This community is dynamic and known to vary in normal individuals with age, ethnicity, diet, exposure to chemicals and also host genetic variation [
6‐
9]. Studies analyzing the gut microbiomes of twins established a link between human genotype and the composition of the gut microbiome [
7]. All these factors make the very definition of a normal core microbiome a great challenge. Aberrations from the normal core microbiome is referred to as “dysbiosis” (meaning imbalance in the microbiome) and has been implicated in auto-immune diseases like diabetes, rheumatoid arthritis, muscular dystrophy, multiple sclerosis and fibromyalgia, in inflammatory diseases like obesity, neonatal necrotizing enterocolitis, inflammatory bowel disease and vaginosis, in some cancers and mental disorders [
10,
11]. Ability of the gut microbiome to modulate the immune system is considered as an important reason for the diseased state [
12]. The direct evidence that the microbiota are indeed the cause of the disease is strengthened by the pioneering studies on obesity in mice. Gut bacteria from fat mice when transplanted into genetically lean mice with no gut bacteria of their own, transform the lean mice into obese mice [
13,
14]. Subsequent studies demonstrated that skinny germ free mice plump up on receiving a fecal transplant from a human donor implying that the bacteria help the recipient to digest and metabolise more efficiently [
13‐
15]. But, if the fecal transplant of the human donor was supplemented with
Christensenella minuta the recipient mice were thinner indicating that
C. minuta controls obesity [
7]. Another example, emphasizing the role of gut bacteria is related to
Clostridium difficile infection (CDI) patients who are cured of CDI when transplanted with fecal microbiota from normal individuals [
16,
17]. This led to the concept that just as a pathogen could cause a disease a “good” microbe could prevent a disease? For instance
Faecalibacterium prausnitzii could protect mice against experimentally induced intestinal inflammation since these gut bacteria were anti-inflammatory. Yet another example of a good microbe is
Akkermansia muciniphila. Increase in abundance of
A. muciniphila correlated with an improved metabolic profile and reversed obesity and decreased insulin resistance probably mediated by endocannabinoids secreted by
A. muciniphila [
18,
19].