This sounds like very legitimate information, but I'm not you, nor am I a nutritionist or doc.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0020113 Introduction Growing evidence shows that the composition and diversity of the microbiota in the human intestine can have a surprisingly strong impact on the well-being and health of the host. For example, inflammatory bowel disease (IBD) has been associated with the disturbance of the intestinal microbiota, resulting in the modulation and dysregulation of the inflammatory responses in the intestine [1]. Microbiota composition has been shown to have an effect on the energy harvest and storage of the host [2] and thus, microbiota alterations associated with obesity may have a role in weight-associated health problems.
The microbiota composition in the human intestinal tract is determined by several factors, such as host genotype, health status, age, microbial interactions, and diet [3]. Based on numerous intervention studies, there is convincing evidence for the influence of the diet on the intestinal microbiota (e.g. [4], [5]). In contrast, although growing evidence indicates that host genetic background has a significant impact on the microbiota composition in the intestine, no specific genetic factors determining the intestinal microbiota composition have been established to date. Twin studies applying plate counts, PCR-DGGE fingerprinting or DNA microarrays have shown a higher similarity in the microbiota composition between monozygotic twins than between dizygotic twins, unrelated persons, marital couples and family members [6]–[7], thus clearly pointing to a strong effect of host genetics. In the study by Turnbaugh et al. [8], the pyrosequencing analysis also showed a higher level of similarity in the microbiota composition in twin pairs than between twins and their mothers or unrelated persons, although in their study the similarity of the microbiota between monozygotic twins did not differ from that of dizygotic twins.
The human intestinal tract is colonised with highly diverse and numerous microbiota which has an established role in maintaining the intestinal homeostasis. A particularly interesting group is bifidobacteria, which comprise the predominant intestinal microbiota in infants and are abundant also in the adult population comprising up to 6% of the normal intestinal microbiota [9]. An adult intestine is typically colonised with one to four bifidobacterial species [10], B. longum, B. adolescentis, B. bifidum and B. catenulatum being the most prevalent [11], [12]. Bifidobacteria have beneficial properties, such as immunomodulatory and pathogen inhibition effects (reviewed by [13]). They also are commonly incorporated in probiotic products.
The A, B and H blood group antigens are α1,2-linked fucose containing glycans present on glycoproteins and glycolipids of erythrocytes (red blood cells) in individuals representing A, B and H blood groups, respectively. The enzyme fucosyltransferase 1 encoded by the FUT1 gene is responsible for the synthesis of ABH antigens on erythrocytes. The ABH antigens are also expressed in mucus and other secretions, where their expression is generated by another enzyme, fucosyltransferase 2 (secretor type α1,2-fucosyltransferase) encoded by the FUT2 gene. In ABH secretor individuals (80% of Caucasians) fucosyltransferase 2 converts type 1 N-acetyllactosamine glycan chains to H antigen, which functions as a precursor for the A, B and Lewis b antigens. Non-secretor individuals do not express active fucosyltransferase 2 enzyme due to a non-sense mutation in the FUT2 gene and therefore they are not able to express the ABH antigens in their mucus and other secretions. The FUT2 gene together with the FUT3 gene encoding fucosyltransferase 3 (Lewis type α1,3/4-fucosyltransferase), is also required for the synthesis of Lewis b histo-blood group (Le a−b+) antigens in secretions. In non-secretor individuals, the FUT3 gives rise to the Lewis a histo-blood group (Le a+b−) antigen due to non-functional fucosyltransferase 2. Lewis negative (Le a−b−) individuals have a mutation in FUT3 gene leading to Lewis null phenotype, irrespective of the secretor status or FUT2 gene. These mucosal ABH and Lewis histo-blood group antigens are known to serve as an energy source [14] and adhesion receptors for many microbes [15], and thus could play a role in shaping the microbiota composition of the host.
In the present study, we report that the genetic variation in the human fucosyltransferase 2 (FUT2) gene determining the presence of mucosal α1,2-fucosylated glycan structures, such as ABH and Lewis b histo-blood group antigens, is strongly associated with the microbiota composition, in particular that of bifidobacteria, in the human intestinal tract. We studied the association of the secretor status (determined by the FUT2 gene) with the intestinal microbiota composition by comparing the dominant bacterial and bifidobacterial populations in faecal samples of non-secretor and secretor individuals. The denaturing gradient gel electrophoresis (PCR-DGGE) and qPCR analysis showed that the composition of the intestinal microbiota and particularly bifidobacteria was strongly associated with the host's secretor status. Secretor status determining the expression of the ABH and Lewis b glycan epitopes in the human intestine seems to be one of the host features significantly shaping the composition of bifidobacteria in the intestine.
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