How does our Western diet influence Crohn's?

"Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10−/− mice", Devkota et al. in Nature (2012) Preview"The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health1. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the…"

Milk fat found in junk food may be to blame for dramatic rise in IBS cases

"Concentrated milk fat is a powdery substance that is abundant in processed foods and confectionery.
...
Prof Chang's team found that milk fat, but not polyunsaturated fats, caused an explosion in the numbers of a normally rare gut microbe called Bilophila wadsworthia.

The bugs were almost undetectable in mice on low-fat or unsaturated fat diets, but made up about 6% of all bacteria in the guts of mice fed milk fat.  Bilophila wadsworthia has an affinity for bile, which is released into the intestines to help break down fats.
...
Milk fats are unusually difficult to digest, requiring the liver to produce bile rich in sulphur.

Since B. wadsworthia thrives on sulphur, this fuels its population growth.

'Unfortunately, these can be harmful bacteria,' Prof Chang said.

'Presented with a rich source of sulphur, they bloom, and when they do, they are capable of activating the immune system of genetically prone individuals.'

By-products of the bugs' interaction with bile enhance the effect by making the bowel more permeable, the scientists said.

Immune cells then find it easier to infiltrate the bowel wall and damage tissue.
...
Prof Chang added: 'Right now we can't do much about correcting genes that predispose individuals to increased risk for these diseases, and while we could encourage people to change their diets, this is seldom effective and always difficult." [Emphasis mine.]

Western diet changes gut bacteria and triggers colitis in those at risk

"Bacteria isolated from surgical infections and its susceptibilities to antimicrobial agents--special references to bacteria isolated between April 2009 and March 2010" in The Japanese Journal of Antibiotics (2011)
"We should carefully follow up B. wadsworthia which was resistant to various antibiotics...."

"Diversity and distribution of sulphate-reducing bacteria in human faeces from healthy subjects and patients with inflammatory bowel disease" in FEMS Immunology and Medical Microbiology (2012)
"The relative abundance of different groups of sulphate-reducing bacteria (SRB) in faecal DNA collected before and after therapy from patients suffering from Crohn's disease (CD), irritable bowel syndrome (IBS) or ulcerative colitis (UC) has been compared with that from healthy controls. Growth tests revealed that SRB were not more abundant in samples from patients with CD before treatment than in the healthy control group. ... However, some samples from patients with CD before treatment contained a growth inhibitor that was absent from IBS or UC samples. In-depth sequencing of PCR-generated dsrB fragments revealed that the diversity detected was surprisingly low, with only eight strains of SRB and the sulphite-reducing bacterium, Bilophila wadsworthia, detected above the 0.1% threshold. The proportion of the two major species detected,B. wadsworthia and Desulfovibrio piger, was as high as 93.5% of the total SRB population in the healthy control group and lower in all patient groups."

Does a Western Diet cause and/or worsen Crohn's?

Loren Cordain - Origins and Evolution of the Western Diet: Health Implications for the 21st Century. - YouTube: ""

Does carrageenan worsen Crohn's?

Carageenan explained in Wikipedia

• extracted from red seaweed (Rhodophyceae family)
• sulphated
• oligosaccharide (polymeric carbohydrate)
• in the food industry, carrageenans are used as stabilizers, thickners, texturizers, emulsifiers, gelation, suspension, water binding, texture enhancers

• processed foods with carrageenan include:  deli meat, hams, chocolate milk, ice cream, sour cream, butter milk, cottage cheese, egg nog, evaporated milk, soy milk, infant formula, water gel, puddings, flan, pie fillings, toaster pastries, fruit toppings, frust syrups, fruit strips, cheese sauces, cake glazes, batters, frozen dough (see Ingredients Solutions for more info)
• kappa-carrageenan has properties of gel and is used in breading and batter
• kappa2-carrageenan has properties of gelling and thickening and is used primarily for milk
• lambda carrageenan has binding properties, helps to retain moisture, and contributes to viscosity and is used in sweet doughs and to thicken dairy products
• iota carrageenan has gel properties and is used in fruit products
• carrageenan degrades with  high heat and acidity
• degraded carrageenan is called polygeenan

"Review of harmful gastrointestinal effects of carrageenan in animal experiments", Tobacman in Environ Health Perspect (2001)
" Review of these data demonstrated that exposure to undegraded as well as to degraded carrageenan was associated with the occurrence of intestinal ulcerations and neoplasms. This association may be attributed to contamination of undegraded carrageenan by components of low molecular weight, spontaneous metabolism of undegraded carrageenan by acid hydrolysis under conditions of normal digestion, or the interactions with intestinal bacteria. ... Because of the acknowledged carcinogenic properties of degraded carrageenan in animal models and the cancer-promoting effects of undegraded carrageenan in experimental models, the widespread use of carrageenan in the Western diet should be reconsidered." [emphases mine]

c.f. "A critical review of the toxicological effects of carrageenan and processed eucheuma seaweed on the gastrointestinal tract", Cohen in Crit Rev Toxicol (2002)
"Carrageenan is not degraded to any extent in the gastrointestinal tract and is not absorbed from it in species examined, such as rodents, dogs, and non-human primates. Systemically administered carrageenan has been reported to have a variety of effects, particularly on the immune system, but these are not pertinent to orally administered carrageenan. The substance poligeenan (formerly referred to as degraded carrageenan) is not a food additive. It exhibits toxicological properties at high doses that do not occur with the food additive carrageenan. In-long term bioassays, carrageenan has not been found to be carcinogenic, and there is no credible evidence supporting a carcinogenic effect or a tumor-promoting effect on the colon in rodents. Also, like many dietary fibers, there is significant cecal enlargement in rodents when it is administered at high doses, but this does not appear to be associated with any toxicological consequences to the rodent. Many toxicological studies on carrageenan have involved administration at doses in excess of today's standards for dietary feeding levels in bioassays, and they are orders of magnitude in excess of those to which humans are exposed."

"Carrageenan: Response", Tobacman, Environmental Health Perspectives (2002)
"It is difficult to recognize a wolf in sheep's clothing. This seems to be the situation with regard to carrageenan. ... Extensive experimental data have demonstrated that a) degraded carrageenan produces neoplasms and ulcerations in animal models; b) acid hydrolysis, such as occurs in the stomach, leads to the production of degraded carrageenan from food-grade carrageenan; and c) food-grade carrageenan contains significant amounts of degraded carrageenan. Human consumption of carrageenan has been increasing steadily in the United States in the 20th century."

"A 90-day dietary study on kappa carrageenan with emphasis on the gastrointestinal tract", Weiner et al. in Food Chem Toxicol (2007)
"Clinical signs were limited to soft feces in high dose rats and to a lesser extent in low dose rats. There were no treatment-related effects on body weights, urinalysis, hematology or clinical chemistry parameters, or on organ weights or ophthalmic, macroscopic or microscopic findings."

"Degraded carrageenan causing colitis in rats induces TNF secretion and ICAM-1 upregulation in monocytes through NF-kappaB activation" in PLoS One (2010)
From Abstract:  "Carrageenan (CGN) is a high molecular weight sulphated polysaccharide derived from red seaweeds. In rodents, its degraded forms (dCGN) can induce intestinal inflammation associated with macrophage recruitment and activation.  ... These data strongly suggest that the degraded forms of CGN have a pronounced effect on monocytes, characteristic of an inflammatory phenotype." [emphasis mine]
"All rats developed diarrhea during degraded carrageenan administration and gross evidence of blood was frequently detected in the stools. ... Histological examination revealed various degrees of mucosal inflammation. ... More severe mucosal injuries including ulceration, hyperplastic epithelium, crypt distortion and a strong macrophage infiltration, were observed in the 40 kDa dCGN-treated rats. ... Treatment with dCGN also induced a strong aggregation of monocytes, detected by phase contrast inverse microscopy (Fig. 5). Although this effect was easily observed in monocytes incubated with the 10 kDa dCGN (Fig. 5B), a more robust cell aggregation was observed in monocytes incubated with the 40 kDa dCGN.  ...  Although native form CGN (200–800 kDa) has been declared harmless to humans [8], its degraded forms (<50 kDa), also known as poligeenan, are widely used to induce colitis in rodents [3]–[5]. These degraded CGN may also have a possible carcinogenic effect [4], [6]–[8]; however this is still controversial. ...  it is probable that some dCGN are produced by acid hydrolysis during gastric digestion [9], [10] or interaction with intestinal bacteria [11], [12]. Thus, understanding the mechanisms of dCGN-induced bowel inflammation is of great importance. In this report, we have analyzed the role of human monocytes (PBM and THP-1) in dCGN-induced inflammation. ... Preliminary in vivo studies in rats treated with dCGN revealed significant shortening of the large intestine associated with an inflammatory state, i.e. strong infiltration of macrophages to the intestinal mucosa similar to DSS-induced inflammation. ... These results suggest that monocytes might produce cytokines associated with activation into macrophages in response to dCGN. ... [I]t is possible that TLR4 is activated by dCGN to induce cytokine secretion by monocytes. ... Thus, degraded CGN clearly can activate monocytes to express an increased number of ICAM-1 adhesion molecules, therefore being capable of creating the conditions characteristic of Crohn's disease symptomatology, i.e. PBM accumulation and MGC formation. ... We presume that the differential effects of 10 and 40 kDa dCGN to induce these effects on monocytes are tightly linked to their capacity to induce inflammation in vivo. However, in vivo, macrophages do not come in direct contact with the intestinal lumen and are separated by the epithelial barrier. The way by which dCGN may leave the intestinal lumen and cross the epithelial barrier to reach the macrophages is an intriguing open question. One possible explanation resides in the potential of dCGN to “induce” cellular and paracellular injurious effects at the intestinal epithelial cell monolayer. ... These results suggest that, although CGN is widely used as a food additive, its degraded forms have an important effect on monocytes characteristic of an inflammatory phenotype." [emphases mine]

Carrageenan and the Acceptance of Food Additive Toxicity, 1950-2000 by Mariel Wolfson (2008), published on SCD Recipes