Another reason why it's so critical to control your gut environment. Pathogenic bacteria is more and more not only connected to obesity and mental illness (especially depression), but now links to cancer.
Güt Health, especially with the new double strength formula, helps prevent pathogenic bacteria from gaining a foothold on the enteric sites, and instead pass harmlessly through you. AS well, the Zinc-l-carnosine bolsters the mucous membrane, another barrier to pathogenic access to the bloodstream.
Make no mistake about it, this IS a war that we are all in Make sure your firepower is superior.
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Cancer Discov. 2017 Feb 15. pii: CD-16-0932. doi: 10.1158/2159-8290.CD-16-0932. [Epub ahead of print]
Gut Microbiota Promotes Obesity-Associated Liver Cancer through PGE2-Mediated Suppression of Antitumor Immunity.
Loo TM1, Kamachi F1, Watanabe Y1, Yoshimoto S2, Kanda H3, Arai Y1, Nakajima-Takagi Y4, Iwama A4, Koga T5, Sugimoto Y5, Ozawa T1, Nakamura M1, Kumagai M1, Watashi K6, Taketo MM7, Aoki T8, Narumiya S8, Oshima M9, Arita M10, Hara E2, Ohtani N11.
Author information
Abstract
Obesity increases the risk of cancers, including hepatocellular carcinomas (HCCs). However, the precise molecular mechanisms through which obesity promotes HCC development are still unclear. Recent studies have shown that gut microbiota may influence liver diseases by transferring its metabolites and components. Here, we show that the hepatic translocation of obesity-induced lipoteichoic acid (LTA), a Gram positive gut microbial component, promotes HCC development by creating a tumor-promoting microenvironment. LTA enhances the senescence-associated secretory phenotype (SASP) of hepatic stellate cells (HSCs) collaboratively with an obesity-induced gut microbial metabolite, deoxycholic acid (DCA) to upregulate the expression of SASP factors and cyclooxygenase-2 (COX-2) through Toll-like receptor (TLR) 2. Interestingly, COX-2-mediated prostaglandin E2 (PGE2) production suppresses the antitumor immunity through EP4 receptor, thereby contributing to HCC progression. Moreover, COX-2 overexpression and excess PGE2 production were detected in HSCs in human HCCs with non-cirrhotic, non-alcoholic steatohepatitis (NASH), indicating that a similar mechanism could function in humans.
Copyright ©2017, American Association for Cancer Research.
PMID:
28202625