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Enhancing the Communication Between Your Microbiota and Your Body is Important

Your health is dependent upon the communication between the community of organisms in your gut (microbiota) and your body. This communication is known as Inter-Kingdom cell to cell signaling (Huges & Sperandio, 2008). 

In other words, probiotic and other helpful organisms do more good work than you think! These organisms create a favorable gut environment that contributes to essential communications to positively effect different organs in your body.

But when this equilibrium between organisms and your body is disrupted, the body somehow has to face the stressors (bad diet, medications, toxins etc.) and it does through various means, one of them is Autophagy

Autophagy is your body's own "cleaning mechanism," a  clearing out of damaged cells, a process that is also responsible to preventing diseases to occur such as autoimmune to infection diseases and others (Lapaquette et al., 2021).  

Keeping the gut microbiota or the community of organisms in your guy healthy is important. Check out the Original Synbiotic, a broad spectrum probiotic formula with prebiotic. 


A symbiotic relationship has set up between the gut microbiota and its host in the course of evolution, forming an interkingdom consortium. The gut offers a favorable ecological niche for microbial communities, with the whole body and external factors (e.g., diet or medications) contributing to modulating this microenvironment. Reciprocally, the gut microbiota is important for maintaining health by acting not only on the gut mucosa but also on other organs. However, failure in one or another of these two partners can lead to the breakdown in their symbiotic equilibrium and contribute to disease onset and/or progression. Several microbial and host processes are devoted to facing up the stress that could alter the symbiosis, ensuring the resilience of the ecosystem. Among these processes, autophagy is a host catabolic process integrating a wide range of stress in order to maintain cell survival and homeostasis. This cytoprotective mechanism, which is ubiquitous and operates at basal level in all tissues, can be rapidly down- or up-regulated at the transcriptional, post-transcriptional, or post-translational levels, to respond to various stress conditions. Because of its sensitivity to all, metabolic-, immune-, and microbial-derived stimuli, autophagy is at the crossroad of the dialogue between changes occurring in the gut microbiota and the host responses. In this review, we first delineate the modulation of host autophagy by the gut microbiota locally in the gut and in peripheral organs. Then, we describe the autophagy-related mechanisms affecting the gut microbiota. We conclude this review with the current challenges and an outlook toward the future interventions aiming at modulating host autophagy by targeting the gut microbiota. Article 

Original Synbiotic 

Original Synbiotic 

 Suggested use: One teaspoon by mouth (very tasty) or mixed in a little water. 


  • Lapaquette, P., Bizeau, J. B., Acar, N., & Bringer, M. A. (2021). Reciprocal interactions between gut microbiota and autophagy. World Journal of Gastroenterology27(48), 8283. Article
  • Autophagy: Glick, D., Barth, S., & Macleod, K. F. (2010). Autophagy: cellular and molecular mechanisms. The Journal of pathology221(1), 3-12. Article
  • Hughes, D. T., & Sperandio, V. (2008). Inter-kingdom signalling: communication between bacteria and their hosts. Nature Reviews Microbiology6(2), 111-120. Article

    Sincerely yours,


    We have developed our products based on scientific research and/or the practical experience of many healthcare practitioners. There is a growing body of literature on food based nutrition and supplements and their application in support of our health. Please use our products under the advisement of your doctor.

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     And more on Inter-Kingdom communication:

    Hughes, D. T., & Sperandio, V. (2008). Inter-kingdom signalling: communication between bacteria and their hosts. Nature Reviews Microbiology, 6(2), 111-120. Article

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