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Emulsifiers destroy intestinal flora

emulsifier ibd ibs obesity

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#1 Kalliste

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Posted 28 February 2015 - 08:06 AM


I guess most people on here are already weary of food additives. I've tried to stay away from light products for a couple of years but I mostly did that believing that fat was an important part, maybe fat is not all that important but emulsifiers are much worse.

 

http://www.nature.co...ature14232.html

http://www.medicalda...-obesity-323528

The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota–host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine1. Thus, agents that disrupt mucus–bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro2, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century3. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host–microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.

 


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#2 FunkOdyssey

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Posted 01 March 2015 - 12:58 AM

I wonder: do natural emulsifiers like egg lecithin and soy lecithin have a similar effect?


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#3 Darryl

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Posted 01 March 2015 - 07:21 PM

The thread title is a bit off, as the emulsifiers altered species composition, increasing some believed beneficial (Akkermansia muciniphila), as well as pathobionts (Proteobacteria). Its not clear that the proinflammatory effects were entirely mediated by changes in intestinal flora, as in a prior (uncited) study just adding soy lecithin to a single meal increased postprandial endotoxemia, and numerous studies indicate commensal endotoxins and their TLR-4 receptor are involved in experimental metabolic syndrome with high-fat feeding, even in the absence of emulsifiers.

 

Laugerette F et al. Emulsified lipids increase endotoxemia: possible role in early postprandial low-grade inflammationThe Journal of nutritional biochemistry. 2011: 22(1), 53-59.

 

In the present study, we first investigated in humans the impact of a mixed meal containing dispersed lipids on postprandial endotoxemia and inflammation. We then investigated the effect of (i) oil emulsification in vivo in rats and (ii) fatty acid amounts in vitro using Caco-2 cells on postprandial endotoxemia. In humans, postprandial endotoxemia increased early after the meal. Moreover, we evidenced that the endotoxin receptor sCD14 increased during digestion and that chylomicrons could contribute to absorbed endotoxin transport. This could explain the significant peak of inflammatory cytokine IL-6 that we observed 2 h after the mixed meal. Interestingly, in rats, the emulsion led to both higher endotoxemia and hypertriglyceridemia than oil and compared to a control saline load.

 

Rats were randomly assigned to an experimental group and received 2.4 ml of one of the three following diets: physiological saline; 50% (v/v) sunflower oil +50% (v/v) physiological saline; or a fine emulsion of sunflower oil in physiological saline using soybean lecithin.

 

The higher increase in postprandial lipemia with the emulsion compared to free oil can be partly explained by their difference in fat surface area which is known to enhance lipolysis and postprandial lipemia. It may also be due to the presence of phospholipids (lecithin) that are known to increase lipid absorption and chylomicron secretion. Consistently, previous in vitro and in vivo studies have also shown that the degree of fat emulsification and the type of emulsifier can impact on digestive lipolysis and digestion kinetics.

 

See also:

 

Erridge C et al. A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. The American journal of clinical nutrition. 2007: 86(5), 1286-1292.
Ghoshal S et al. Chylomicrons promote intestinal absorption of lipopolysaccharides. Journal of lipid research. 2010: 50(1), 90-97.
Pendyala S et al. A high-fat diet is associated with endotoxemia that originates from the gut. Gastroenterology. 2012: 142(5), 1100-1101.

Edited by Darryl, 01 March 2015 - 07:52 PM.






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