Berries Improve Gut Health and are Protective Against Neuroinflammation!

Experts believe that gut dysbiosis is a cause of environmental illness. Changes in the gut biome can be caused by antibiotic use, environmental insults from chemicals in food and water and high fat and high sugar diets. These changes lead to morphological changes in the wall of the intestines that allows for easier translocation of harmful bacteria. It is believed that translocation may be one significant cause of chronic fatigue syndrome. In addition, it is believed that dysbiosis may lead to neuroinflammation that is believed to be a major source of symptoms in chronic fatigue and fibromyalgia.

Numerous studies published in the recent past have shown that consumption of some fruits and herbs may improve gut health. Research has demonstrated that anthocyanins in berries may counteract dysbiosis. In addition, they also have anti-neuroinflammatory properties and allow for better communication between the gut and the brain. Lastly, they alter tryptophan metabolism increasing the neuroprotective metabolite kynurenic acid. (1) Incidentally, this pathway also produces the antioxidant 3-hydroxyanthranilic acid which inhibits inflammatory proteins by activating Nrf2. (2) 





1. Gut microbiota modulation accounts for the neuroprotective properties of anthocyanins. Scientific reports, Vol. 8, No. 1. (27 July 2018) by Cláudia Marques, Iva Fernandes, Manuela Meireles, et al.

2. 3-Hydroxyanthranilic acid, one of L-tryptophan metabolites, inhibits monocyte chemoattractant protein-1 secretion and vascular cell adhesion molecule-1 expression via heme oxygenase-1 induction in human umbilical vein endothelial cells. Atherosclerosis, Vol. 187, No. 2. (August 2006), pp. 274-284 by Hyun-Ock O. Pae, Gi-Su S. Oh, Bok-Soo S. Lee, et al.

Smoking Promotes Pathogen Colonization and Translocation in the Respiratory Tract!

"A study from last year found that Haemophilus influenzae, a gram-negative bacteria that is responsible for infections, drives the development of COPD when combined with cigarette smoking. Also, exacerbations of COPD occur when provoked by bacterial strains from the environment. In a follow-up study, the authors wanted to further examine if cigarette smoke promotes colonization of lung pathogens in the respiratory tract and if colonization linked to inflammation. As a result of this study, researchers were able to demonstrate that cigarette smoke increased the number of H. influenzae in the upper airways while clean air did not. In addition, the presence of S. pneumoniae was enhanced in the upper respiratory tract of mice exposed to cigarette smoke and accompanied by increased translocation of S. pneumoniae in the lung.  The author's determined that cigarette negatively impacts the ability for a "host" to  control colonization of the upper respiratory tract that results in increased inflammation and the translocation of bacteria in the lungs. "

Cigarette smoke-promoted acquisition of bacterial pathogens in the upper respiratory tract leads to enhanced inflammation in mice. Respiratory research, Vol. 16, No. 1. by Meike Voss, Bodo Wonnenberg, Anja Honecker, et al. http://www.citeulike.org/user/kimberlykramer2015/article/13586550

Combined exposure to cigarette smoke and nontypeable Haemophilus influenzae drives development of a COPD phenotype in mice. Respiratory research, Vol. 15 (2014) by Shyamala Ganesan, Adam T. Comstock, Brenton Kinker, et al. http://www.citeulike.org/user/kimberlykramer2015/article/13586551