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Intestinal dysbiosis and circadian rhythm disruption are associated with similar diseases including obesity, metabolic syndrome, and inflammatory bowel disease.[1] Despite the overlap, the potential relationship between circadian disorganization and dysbiosis is unknown; thus, in the present study, a model of chronic circadian disruption was used to determine the impact on the intestinal microbiome. Male C57BL/6J mice underwent once weekly phase reversals of the light: dark cycle (i.e., circadian rhythm disrupted mice) to determine the impact of circadian rhythm disruption on the intestinal microbiome and were fed either standard chow or a high-fat, high-sugar diet to determine how diet influences circadian disruption-induced effects on the microbiome.

Our gut as we all know is home to innumerable different bacteria — a complex ecosystem that has an active role in a variety of bodily functions. In a study published on the 13th May 2013 in Proceedings of the National Academy of Sciences,[1] a team of researchers finds that in mice, just one of key bacterial species plays a major part in controlling obesity and metabolic disorders such as type 2 diabetes.

The bacterium, unfamiliar to many of us and called Akkermansia muciniphila, digests the epithelial mucus and makes up 3–5% of the microbes in a healthy mammalian gut. But the intestines of obese humans and mice, and those with type 2 diabetes, have much lower levels. The researchers led by Patrice Cani, who studies the interaction between gut bacteria and metabolism at the Catholic University of Louvain in Belgium, decided to investigate the link.

In January 2011 a very interesting paper was published in Physiological Reviews, exploring the role of gastrointestinal permeability, genetics and risk of development of autoimmune diseases.[1]

This abstract explores some of the principle messages in the paper which is also available as a full free text.

It is generally accepted that it is the interplay between environmental factors and specific susceptibility genes that underlies the aberrant immune response responsible for the onset of these diseases. Less than 10% of those with increased genetic susceptibility progress to clinical disease, suggesting a strong environmental trigger in the predisease state.

A possible link between what a mother eats during pregnancy and the risk of her child developing allergies has been identified in new research published in Septembers; The Journal of Physiology.[1]

This paper identified that if the maternal diet is rich in PUFA’s or poly unsaturated fats such as those found in flaxseed, walnuts and fish their offspring’s digestive tract develops differently than in those progeny lacking these PUFAs.

Leaky Gut Induces Visceral Obesity

Wednesday, 09 November 2011 by | Comments: 2

From its dark days as a concept dismissed by most Drs and scientists as being suitable only for the more eccentric alternative medicine crowd, the idea that the gastrointestinal tract may have varying levels and quality of exclusionary capacity has slowly become mainstream-ish.

A paper out in the prestigious Nature Journal – Obesity, has raised the question that altered visceral adiposity – ‘fat around the middle’ may be initiated and promoted by altered barrier integrity.[1]

There are questions in the literature, at Dr’s Surgeries, in hospitals and in clinics relating to the existence of gluten generated problems including, increased gut permeability and gastrointestinal symptoms in patients that do not diagnostically qualify as being coeliac.

In fact many people will state they are aware that not eating gluten helps them, and aids well -being , and may even resolve quite significant physical distress. They note recovery on a GFD and yet still have problems achieving medical and family support for their activities.

As part of a nutritional strategy to impart improvements to mucosal barrier in compromised patients the use of a naturally occurring growth factor has been explored in many studies and in some supplements in clinical use. Glandular extract derived from bovine sources that contributes epithelial growth factor (EGF) offer an additional strategy for epithelial tissue repair. EGF is a normal constituent of saliva production during the act of eating, is also secreted into the gut lumen and found in colostrum and milk. The purpose is to aid in the management of epithelial tissue health and it is naturally degraded by pancreatic enzymes during digestion.

The amino acid L-Arginine is suspected through animal models to increase intraluminal production of EGF and may explain why this protein is a useful method for repairing intestinal damage.[1]

LGG Attenuates Barrier Permeability In The Gut

Tuesday, 13 July 2010 by | Comments: 1

Increased gut permeability as discussed in other posts has been linked with symptoms far from the gut and include depression, arthritis, diabetes and other conditions in which a pro inflammatory milieu is being maintained. Some immunologists now refer to this low grade inflammation as Para-Inflammation. Locally, the barrier defect can contribute to diahorrhea and chronic inflammatory bowel diseases.

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Michael Ash looks at leaky gut with a contemporary approach to investigation, relevance and restoration. It is quite clear that in order to extract nutrients and other sentinel information carrying agents the barrier that divides the contents of the gastric lumen from the host must be permeable. The question that has interested clinicians for many years is – when is it too permeable and what does that mean in terms of health and illness.

A paper in the March edition of Mucosal Immunology explores this concept in some detail and delivers some much needed information and potential direction in terms of dietary management and risk.[1]

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