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Dysbiosis: A Game Changer in the Body’s Overall Health Regulation

Submitted by on September 1, 2016 – 9:10 PM

good-vs-bad-bacteria-cartoonIn my last blog post about the gut, I mentioned the role that our GIT bacteria play in regulating various physiological processes. Current research reveals that the influence they have on our body is unfathomable; “dysbiosis,” referring to abnormalities in these GIT bacteria, is found to have far-reaching clinical implications with regard to diseases such as Autism Spectrum Disorder (ASD), Parkinson’s disease (PD) and others.

A study published in the journal Cell reported that a high-fat diet given to maternal mice was associated with autism-like symptoms in the mice offspring. It is believed that the high-fat diet causes a reduction in certain key GIT Bacteria; specifically Lactobacillus reuteri. The study showed that this bacteria, Lactobacillus reuteri, promotes production of oxytocin in the paraventricular nuclei of the hippocampus.

Oxytocin is known for its role in inducing uterine contractions and breast milk release, but it also additionally contributes to social recognition, pair bonding and maternal behaviors. It is possible that a decrease in oxytocin caused by this dysbiosis of Lactobacillus reuteri causes the social symptoms characteristic of Autism Spectrum Disorder by interfering with the normal pair bonding/social recognition functions mediated by this hormone. Other studies linking ASD to GIT dysbiosis have shown probiotic treatment to reduce some of the aforementioned symptoms.

Furthermore, a significant proportion of Parkinson’s patients exhibit GIT symptoms—most commonly constipation—years before the onset of motor deficits characterizing PD. The deposits of Lewy bodies/alpha synuclein that typically occur in the CNS of PD patients have also been found in the Enteric Nervous System (ENS) of the gut.

In a review article published in Nature reviews: Neurology, it was shown that these alpha synuclein/Lewy bodies spread via cell to cell transport between neurons making up the ENS. In doing so, they travel caudo-rostrally up to the brain where they deposit in the substantia nigra, thereby leading to the classical motor symptoms of PD. They may spread further into the cortex to cause further cognitive decline. The origin of these Lewy bodies in the GIT may be from environmental factors such as pesticides, herbicides and metals—all known risk factors for PD.

 

All of these findings go to show how significant an impact our GIT Bacteria can have on our cognitive well-being. This is undermined by the ease with which practitioners administer broad-spectrum antibiotics, which can seriously alter the normal gut ecosystem. It has been well established that our gut bacteria affect our immune responses and have a role in immune regulation of various organs, especially the brain.

Research on mice showed that antibiotic-mediated disruption of normal gut bacteria caused a decrease in Ly6Chi monocytes, immune cells that act as messengers between the gut and brain. This decrease in Ly6Chi monocytes led to a decrease in brain neurogenesis and its associated cognitive decline. Recovery of these cells, by exercise or probiotic supplementation, was able to reverse the effects of decreased neurogenesis.

 

References:

  • Buffington, S. A., Di Prisco, G. V., Auchtung, T. A., Ajami, N. J., Petrosino, J. F., & Costa-Mattioli, M. (2016). Microbial Reconstitution reverses maternal diet-induced social and Synaptic deficits in offspring. Cell, 165(7), 1762–1775.
  • Bresnahan, M., Hornig, M., Schultz, A. F., Gunnes, N., Hirtz, D., Lie, K. K., … Lipkin, W. I. (2015). Association of maternal report of infant and toddler gastrointestinal symptoms with autism. JAMA Psychiatry, 72(5), 466
  • Klingelhoefer L, & Reichmann H (2015). Pathogenesis of Parkinson disease-the gut-brain axis and environmental factors. Nature reviews. Neurology, 11(11), 625-36
  • Ulusoy A, Rusconi R, Pérez-Revuelta BI, Musgrove RE, Helwig M, Winzen-Reichert B, & Di Monte DA (2013). Caudo-rostral brain spreading of ?-synuclein through vagal connections. EMBO molecular medicine, 5(7), 1051-9
  • Lai BC, Marion SA, Teschke K, & Tsui JK (2002). Occupational and environmental risk factors for Parkinson’s disease. Parkinsonism & related disorders, 8(5), 297-309
  • Bercik P, & Collins SM (2014). The effects of inflammation, infection and antibiotics on the microbiota-gut-brain axis. Advances in experimental medicine and biology, 817, 279-89
  • Möhle, L., Mattei, D., Heimesaat, M., Bereswill, S., Fischer, A., Alutis, M., French, T., Hambardzumyan, D., Matzinger, P., Dunay, I., & Wolf, S. (2016). Ly6Chi Monocytes Provide a Link between Antibiotic-Induced Changes in Gut Microbiota and Adult Hippocampal Neurogenesis Cell Reports, 15 (9), 1945-1956

 

 

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