I hope you have taken a look at the April 2018 newsletter. If not, here is a recap of a great article therein about the INTERSTITIUM, the cells that line all organs. It has been upgraded to an organ itself because of its critical function. When those cells TOIL, that is, when they are Toxic, Oxidized, Inflamed, and have Less than optimal mitochondrial function they become LEAKY. Think of Leaky Gut. Well, we also have Leaky Brain, Leaky Arteries. Practically all organs leak when we eat refined/processed diets, live in toxic environments, and do not handle stress well.
BTW, cholesterol is critical in healing the cells lining those organs. In other words, cholesterol heals leaky organs. If you don’t eat a plant-based diet, you will leak, and may sink. It cannot be overstated: if you are leaking, particularly at the gut level, you will see practically all diseases get started. At first, at the microscopic level when your tests are still normal. Then, you will notice gut issues, and pretty soon you will have metabolic, arthritic, and many other health problems, including cancer.
So, what is the worst “food” associated with Leaky Gut? SUGAR!!!
Scientists identify interstitium as an organ
“TIME (3/27, Park) reports scientists have proposed there is an organ called the interstitium “that may play a critical role in how many tissues and other organs do their jobs, as well as in some diseases like cancer.” The article explains that the interstitium “is a series of connected, fluid-filled spaces found under skin as well as throughout the gut, lungs, blood vessels and muscles.” Newsweek (3/27, Gander) reports the study, which was published in Scientific Reports, marks the “first time” that the interstitium “has been identified as an organ. CNN (3/27, Howard) reports that Neil Theise, MD, one of the study’s authors, said that the interstitium should be considered an organ, because it has a unitary structure and a unitary function. Dr. Theise said, “This structure is the same wherever you look at it, and so are the functions that we’re starting to elucidate.”
Intestinal barriers protect against disease
J. Science 09 Mar 2018:359;1097-1098
“All body surfaces and cavities are lined by layers of epithelial cells, which are connected by cell-cell junctions. These junctions serve three main purposes: adhesion, to maintain tissue integrity; creation of a barrier, to control the passage of ions, water, molecules, cells, and pathogens across epithelial layers; and signaling, to receive and transmit cues that affect cell behavior and tissue function. The barrier function is crucial to maintaining tissue homeostasis. Breaking or even slightly perturbing epithelial barriers can lead to serious pathological consequences, including infection and inflammation (1–3). The intestinal epithelial barrier is constantly being challenged by the gut microbiome, and is leaky in patients with inflammatory bowel disease (IBD). Three studies now characterize how gut epithelial barrier dysfunction is involved in IBD, autoimmune disease, and systemic infection, respectively. Mohanan et al. describe how inactivation of the IBD susceptibility gene, C1orf106 (chromosome 1 open reading frame 106), leads to decreased intestinal barrier function, thereby promoting intestinal inflammation and thus IBD. Manfredo Vieira et al. show how pathogenic bacteria can induce intestinal barrier defects and translocate to lymph nodes and liver, triggering systemic autoimmune disease, such as systemic lupus erythematosus (SLE). Additionally, Thaiss et al. report that hyperglycemia (high blood glucose concentration), which is common in people with obesity, diabetes, and other metabolic syndromes, disrupts the intestinal barrier, leading to intestinal inflammation and systemic infection complications.
Hyperglycemia drives intestinal barrier dysfunction and risk for enteric infection
J. Science 23 Mar 2018:359;1376-1383
“Metabolic syndrome often accompanies obesity and hyperglycemia and is associated with a breakdown in the integrity of the intestinal barrier and increased risk of systemic infection. Thaiss et al. found that mice with systemic infection of a Salmonella analog, Citrobacter rodentium, also exhibited hyperglycemia. Deletion of the glucose transporter GLUT2 altered sensitivity to chemically induced epithelial permeability and protected mice from pathogen invasion. The authors also found a correlation in humans between glycated hemoglobin (an indicator of hyperglycemia) and serum levels of pathogen recognition receptor ligands. Obesity, diabetes, and related manifestations are associated with an enhanced, but poorly understood, risk for mucosal infection and systemic inflammation. In mouse models of obesity and diabetes that hyperglycemia drives intestinal barrier permeability, through GLUT2-dependent transcriptional reprogramming of intestinal epithelial cells and alteration of tight and adherence junction integrity. Consequently, hyperglycemia-mediated barrier disruption leads to systemic influx of microbial products and enhanced dissemination of enteric infection. Treatment of hyperglycemia, intestinal epithelial–specific GLUT2 deletion, or inhibition of glucose metabolism restores barrier function and bacterial containment. In humans, systemic influx of intestinal microbiome products correlates with individualized glycemic control, indicated by glycated hemoglobin levels. Together, our results mechanistically link hyperglycemia and intestinal barrier function with systemic infectious and inflammatory consequences of obesity and diabetes.”
The microbiome in cancer immunotherapy: Diagnostic tools and therapeutic strategies
J. Science 23 Mar 2018:359;366-1370
“The fine line between human health and disease can be driven by the interplay between host and microbial factors. This “metagenome” regulates cancer initiation, progression, and response to therapies. Besides the capacity of distinct microbial species to modulate the pharmacodynamics of chemotherapeutic drugs, symbiosis between epithelial barriers and their microbial ecosystems has a major impact on the local and distant immune system, markedly influencing clinical outcome in cancer patients. Efficacy of cancer immunotherapy with immune checkpoint antibodies can be diminished with administration of antibiotics, and superior efficacy is observed with the presence of specific gut microbes. Future strategies of precision medicine will likely rely on novel diagnostic and therapeutic tools with which to identify and correct defects in the microbiome that compromise therapeutic efficacy.