SUMMARY: Don’t be duped into believing diet has nothing to do with your disease, or in preventing disease. When the researchers themselves rethink and change up their own diet to eliminate the ubiquitous food additive emulsifiers because their research is finding serious adverse impact on the gut lining, I want everyone to rethink their emulsifier intake too, for your gut’s health. Meet here, Dr. Andrew Gewirtz and learn about his important work on Microbiome, Emulsifiers, and their association with IBD and Metabolic Syndrome (defined by NIH as having three or more of these factors or you take drugs to control them: High triglyceride level, reduced high-density lipoprotein (HDL) cholesterol, increased blood pressure, elevated fasting blood sugar, & large waist circumference. How concerned should you be about chowing down emulsifiers? Their connection to gut inflammation and microbiome skew at the mucosal level caused Dr. Gewirtz to eliminate such from his and his family’s diet. One tenet of the healing diets — eliminate processed foods — results in the elimination of emulsifiers. Perhaps it is time to reconsider your emulsifier intake too.
WHY ELIMINATE EMULSIFIERS?
Andrew Gewirtz’s studies in mice show that it is a matter of microbiome and microbes when it comes to emulsifiers in the diet.
Feeding mice emulsifiers altered the microbiota microbiome and Gerwirtz found, for mice, they got:
- IBD (for mice with predisposition to this disease), and
- Low-grade or mild intestinal inflammation and metabolic syndrome for mice having normal immune systems. Metabolic syndrome is characterized by increased levels of food consumption, diabetes, hyperglycemia, elevated cholesterol, elevated triglycerides. insulin resistance, and obesity. This work supports earlier findings that low-grade inflammation resulting from an altered microbiota can be an underlying cause of excess eating.
- What’s metabolic syndrome? The National Institutes of Health guidelines diagnose metabolic syndrome if you have three or more of these traits or are taking medication to control them:
- Large waist circumference — a waistline that measures at least 35 inches (89 centimeters) for women and 40 inches (102 centimeters) for men,
- High triglyceride level — 150 milligrams per deciliter,(mg/dL), or 1.7 millimoles per liter (mmol/L), or higher of this type of fat found in blood,
- Reduced high-density lipoprotein (HDL) cholesterol — less than 40 mg/dL (1.04 mmol/L) in men or less than 50 mg/dL (1.3 mmol/L) in women of this “good” cholesterol,
- Increased blood pressure — 130/85 millimeters of mercury (mm Hg) or higher,
- Elevated fasting blood sugar — 100 mg/dL (5.6 mmol/L) or higher.
Gerwirtz’s study suggests that the current means of testing and approval of food additives may not be adequate to prevent use of chemicals that promote diseases driven by low-grade inflammation and/or which will cause disease primarily in susceptible hosts. Actually though, you know by now that low grade inflammation is synonymous with many diseases, and many diseases have signature microbiomes. If you don’t — check out the drop down menu over on the right side bar to see your disease of interest.
Next up for Gewirtz’s animal microbiome emulsifiers findings — these studies are now being extended to human trials led by researcher Dr. Gary Wu, University of Pennsylvania
I am looking forward to the human data. A simulation of emulsifiers in the human gut performed in Belgium has confirmed the inflammation increase observed in the mice. If similar results are obtained in the human trials, such would indicate that emulsifiers play a role in driving the epidemic of obesity, its inter-related consequences and a range of diseases associated with chronic gut inflammation.
Microbiome dysbiosis cause and effect at this time is not clear. Dysbiosis might cause disease as researchers learn more about how the microbiota can influence the host, but diseased states can also lead to changes to the microbiota. Some mechanisms include the addition of medications such as antibiotics as well as microbiome changes resulting from eating habits [think about the emulsifier additives discussed in this post] and bowel function [IBS, SIBO…]. -The gut microbiome in health and in disease, 2016
New restrictions on common ubiquitous emulsifiers would require food processors to scramble for alternatives to maintain texture, appearance, and quality of their foods and beverages; or we get use to understanding what real unadulterated food is supposed to look like… we learn to stir our peanut butter… This is beginning to sound similar to the death knell of trans-fat elimination from countless products.
What are emulsifiers?
Gerwirtz explains: Emulsifiers are a common class of food additives in virtually all processed food. Many are chemicals, and many are synthetic meaning they do not exist in nature such as carboxomethylcellous and polysorbate 80 . They improve texture but mainly their main role is to increase shelf life. Emulsifiers stabilize mixtures (prevents ice crystals for ice cream, keeps cookies or bread soft, salad dressings and other liquids stay blended that otherwise would separate, etc… ) and they are detergents. -Gewirtz interview, the American Microbiome Institute, Episode 3:Emulsifiers in our food with Dr. Andrew Gewirtz, March 2015. Actually, emulsifiers are only one type of food additive; for a complete listing of emulsifiers see the Code of Federal Regulations, Title 21.
Many components in the food system instigate gut inflammation
Diseases such as rheumatoid arthritis (25), colorectal cancer (26), obesity (27), and diabetes (28) as well as cardiovascular disease, IBS, IBD, Clostridium difficile infection have now been associated with microbiome skew.
It only makes sense to look at your diet and rethink those dietary components now known to cause gut inflammation. Some components of diet found associated with gut inflammation in susceptible animal models was summarized in the study, Reciprocal Interaction of Diet and Microbiome in Inflammatory Bowel Diseases. Such included certain types of higher fat (palm, soy and other fats are discussed here — PUFA Omega-6 corn oil was used in this researcher’s work, see full text study here), as well as the Gerwirtz emulsifier studies (the focus of this post), and the artificial sweetener studies. Most all of these can be reasonably eliminated and substituted with anti-inflammatory choices. You can read about the soybean oil, vegetable oil, and corn oil connection to diabetes and metabolic syndrome here. The type of fat consumed and the connection to breast cancer diagnosis can be read here. The conclusions of those posts is that until the dust settles on fat types and disease… just use oils having long term non controverted known benefit such as EVOO (be certain it is not adulterated with the soybean, corn and vegetable oils — see those posts for listings).
Gut inflammatory food substrates are so ubiquitous in today’s food system that It has come to the point that label reading, though it takes time, is worthwhile. Decrease inflammatory instigation in the gut by choosing foods containing ingredients so that you know what they are.
Eating out at restaurants? Why would you drop $20/meal to eat a lot of ingredients that are going to inflame your gut? Choose raw produce for salads including avocado and hard boiled eggs, bring your own EVOO salad based dressing, and tell them to cook your meat/fish using only EVOO. Update: I did not include chicken. Why? Most have non-SCD broth injection. You can go so far as to bring your own seasonings and sea salt to eliminate the anti-clumping additives of their spice blends and spice powders such as garlic powder and onion powder.
How powerful is diet for disease remission & management?
The microbiota also directly affects structures in the gut. Recent studies demonstrated that the fucosylation of glycoproteins, or the permeability of the mucus layer is influenced by the intestinal ecosystem.[52,53]-Reciprocal Interaction of Diet and Microbiome in Inflammatory Bowel Diseases
Look… diet is so powerful that such is being looked at for disease remission either alone or in combination with therapy for IBD. Diet in the pathogenesis and treatment of inflammatory bowel diseases explains: Researchers have learned much about the effects of diet on the mucosal immune system, epithelial function, and the intestinal microbiome… In the future, engineered diets that restrict deleterious components but supplement beneficial nutrients could be used to modify the luminal intestinal environment of patients with IBD; these might be used alone or in combination with immunosuppressive agents, or as salvage therapy for patients who do not respond or lose responsiveness to medical therapies. Stricter diets might be required to induce remission, and more sustainable exclusion diets could be used to maintain long-term remission. This very concept is what Stanford, in 2016, noted in the study they published that found that liberalized SCD after strict adherence maintained remission for IBD.
I am not going into any more detail of the many dietary substrate connections to gut inflammation since the focus of this post is specific for the emulsifiers. You can however find more discussion of the substrate gut inflammation connection below my signature.
Now for the Technicals of Microbiome, Emulsifiers
The key emulsifier researcher, Dr. Andrew Gewirtz (Georgia State University) presented the emulsifier data last month in Miami
#GMFH2016 at the The Fifth Gut Microbiota for Health Summit – Miami – March 5-6, 2016. You can listen to any of the summit expert researcher presentations here, and specifically Dr. Andrew Gewirtz’s emulsifier presentation here.
Read the study at, Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome, see here for the Nature paper, and here for UPenn pdf of the study. A ScienceDaily article on Gerwirtz’s studies can be read here.
Polysorbate 80 (P80) and carboxymethylcellulose (CMC) were fed mice; the emulsifiers disrupted the gut’s mucosal layer and changed the microbiome.
The findings: CMC and PolySorbate 80 induce reduced distance of bacteria to epithelium in mice ; down to less than 10µm. In simpleton, inflammatory species of bacteria came close to the epithelium where they should not be. P80 and CMC eroded the multi-layered mucus membrane that protects the inner gut lining of the digestive tract from the microbiome bacterial penetration. The researchers believe that the compromised mucosal membrane promoted inflammations. Check out the ending slide in Gewirtz’s presentation:
What inflammations were seen for P80 and CMC?
- Those with predisposition to digestive track inflammation experienced severe gut colitis inflammation (they got IBD), and those with a normal immune system had low-grade digestive tract inflammation along with signs of obesity and metabolic syndrome.
- With emulsifiers:
- Bacteria moves into the epithelium and the mucosal layer thins; such is not due to the detergent nature of the emulsifier but rather due to the microbiome composition changes. Some bacteria was in direct contact with the epithelium.
- The microbiome bacterial composition changed; there was an increase in pro-inflammatory bacteria closer to the epithelium which are more flagellated; they express more pro-inflammatory LPS.
- Such happens at emulsifier doses proportionally far less then that which we normally routinely consume.
- Regarding reversibility following emulsifier elimination, Gerwirtz’s presentation here and interview here, conflicts as he notes partial reversal and then complete reversal, respectively. The human studies should tease this out; but you already know that long term diet changes are needed to change up the resilient microbiome.
- From Gerwirtz’s presentation Q&A and this Gerwirtz interview: In germ-free mice, emulsifiers don’t increase inflammation; this suggests that this effect is microbiome mediated. Images show bacteria is deep into the epithelium, right up against gut lining, increasing inflammation. The mucous layer also thins. In germ-free mice there are no changes to mucosa. This strongly suggests that it is NOT the emulsifier directly dissolving the mucus layer and making it thinner. Something else is happening that dissolves the mucus layer and making it thinner.
- Gerwirtz noted the similarities between metabolic syndrome and IBD; both have: Increased expression of similar pro-inflammatory genes (CRP, etc), feature remodeling of adipose tissue, are associated with alterations in gut microbiota, and requires a microbiota (there is no disease in germ-free mice).
- Gerwirtz’s hypothesis is that metabolic syndrome and IBD are both manifestations of disturbance in the gut — microbiota relationship. Check out Gerwirtz’s slides:
Before DIVING MORE INTO TECHNICALS… Compare what a healthy versus unhealthy gut lining looks like:
A picture truly is worth a thousand words when talking about mucin thickness lining, cytokines, and anti-inflammatory and pro-inflammatory cascade. Below and on the left is a healthy intestinal lining; on the right is the unhealthy IBD (although any inflammatory chronic disease could be substituted for a general understanding of the inflammatory cascade though actual cytokines may vary). As strange as it is, understand that the mucin layer disappears as the pro-inflammatory microbiome feeds upon it if you aren’t eating for your trillion. Gerwirtz’s work is showing that the mucin layer thins for mice eating a diet containing emulsifiers. That such is not due to the detergent nature of the emulsifier but rather due to the microbiome composition changes which increase pro-inflammatory bacteria closer to the epithelium which are more flagellated. The flagellated bacteria express more pro-inflammatory LPS, and such happens at emulsifier doses proportionally far less then that which we normally routinely consume.
The above gut lining pictures also depict SCFA (butyrate and antioxidant producers) which are depleted in unhealthy gut linings. It’s incredible but true that IBD patients eating a healing diet, SCD, actually, increases the F.prausnitzii bacteria which is a SCFA producer. See the post, NICE, SCD INCREASED F. PRAUSNITZII… HUGH?!? and now the Walters UC Davis Medical Center study for details. Isn’t it ironic too, that SCD eliminates emulsifiers (albeit many other food substrates unique to IBD intolerances).
Was the amount of emulsifiers Gerwirtz fed the mice comparative to the amount of emulsifiers we consume?
They tested a range of high and low doses of P80 and CMC and learned that inflammation ensued at doses far less than what the US permits in processed foods. The US permits 1.0 percent P80 for food intake whereas 2.0 percent is permitted for CMC. Gerwritz’s mice showed inflammation when given 0.1 percent to 1 percent of P80 and 0.5 percent of CMC. Gewirtz emphasized that because emulsifiers are so ubiquitous in the food system, the amounts of total emulsifiers given the mice were probably less, proportionately to body mass and intake, than most Americans typically consume.
To practically understand these ramifications: Emulsifiers can be included in one processed food up to 2.0 percent for CMC, but we consume many of these servings because this level can be in every processed food you consume. Not only that, but Gerwirtz’s study only looked at one emulsifier being consumed at a time whereas processed foods contain many emulsifiers. The cumulative effect of numerous emulsifiers, which is what many ingest, was not studied, and that total amount would likely be far above those that were studied that showed gut inflammation.
How hard is it to eat foods that eliminate emulsifiers?
Kids are able to do it in clinical trials eating the healing diet Specific Carbohydrate Diet (SCD) (see all the studies in the collage in this post) to induce and maintain remission for IBD. SCD eliminates emulsifiers along with a lot of other inflammatory food substrate… so stop with the negotiation and bellyaching.
In summary: JUST DO YOUR GUT MICROBIOME A FAVOR; ELIMINATE EMULSIFIERS and STOP NUDGING THE MICROBIOME INFLAMMATORY CASCADE OCCURRING IN THE MUCOSAL LINING that looks like that ASSOCIATED WITH IBD and METABOLIC SYNDROME, and only time will tell, what other inflammatory diseases in those with predisposition.
Another great Gewirtz interview with much more technical details of the emulsifier study for those interested is at the American Microbiome Institute, Episode 3:Emulsifiers in our food with Dr. Andrew Gewirtz, March 2015. A bullet-point summary is:
- Before emulsifier work, Gewirtz worked on Toll-like receptor 5 (TLR5). TLR5 is a receptor on cell membranes that detect bacterial flagellun — long, thin, whip-like appendages attached to a bacterial cell that allow for bacterial movement. A lot of flagellated microbes are opportunistic pathogens and TLR5 is the way the innate immune system senses their presence. Gewirtz’s group thought that if you remove TLR5, inflammation would decrease. What they found is that bacteria not normally considered pathogens linger in the the mucosa and sub epithelium and drive chronic inflammatory diseases, and these bacteria still have other inflammatory pathways such as lipopolysaccharides (LPS). “LPS, at physiologically relevant concentrations, causes an increase in intestinal permeability and could play an important role in further deterioration and prolongation of intestinal TJ barrier defect in intestinal permeability disorders and inflammatory diseases of the gut.” Gerwirtz explains: An analogy for removing TLR5 can be the closing of some firehouses. Eventually the firetrucks get to the fire, but damage is worse and it takes more water to put out the fire. Read his paper in Science.
- At 17:50 — Emulsifier history. Working with TLR5, Gewirtz found that the bacteria closer to the epithelium were more flagellated, and they expressed more LPS which activates Toll-like receptor 4 (TLR4). Overall, this bacterial composition change became inherently more pro-inflammatory, and they were closer to epithelium. Genetic factors have remained unchanged relative to the recent time period where inflammatory diseases have risen to epidemic levels. There is a genetic mutation in about 1 in 200, or 250, people who lack TLR5; they are TLR5 knockout humans, homozygeous; so they have a metabolic syndrome phenotype (they have predisposition for diabetic or high cholesterol propensity) but there aren’t enough of these folks, to explain the huge increase in inflammatory disease. What this means is that mice are a reasonable model of the human disease. Gerwitz’s group focused on what factors in environment that interacts with microbiome might be relevant for the changes being seen in the pro-inflammatory bacteria found now to be closer to the epithelium. They knew that diet directly interacts with microbiome, and a literature review found the in vitro emulsifier trans-location of bacteria work by Alexander Swidsinski. See Swidsinski, Alexander, et al. “Bacterial overgrowth and inflammation of small intestine after carboxymethylcellulsose ingestion in genetically susceptible mice. ”Inflammatory bowel diseases 15.3 (2009): 359-364.
- Emulsifiers are common class food additives in virtually all processed food. Many are chemicals, and many are synthetic meaning they do not exist in nature such as carboxomethylcellous and polysorbate 80 . They improve texture but mainly their main role is to increase shelf life. Emulsifiers stabilize mixtures (prevents ice/cream ice crystals for ice cream, keeps cookies or bread soft, salad dressings and other liquids stay blended that otherwise would separate) and they are detergents.
- Images show bacteria is deep into the epithelium, right up against gut lining, increasing inflammation. The mucous layer also thins. In germ-free mice there are no changes to mucosa. This strongly suggests that it is NOT the emulsifier directly dissolving the mucus layer and making it thinner. Something else is happening that dissolves the mucus layer and making it thinner. They are collaborating with a Gentz, Belgium investigator who has a system of in vitro looking at microbiota. The two possibilities they are considering are:
- There may be a change in the microbiome constituency itself (species change that are more aggressive and penetrate the mucus) or
- The emulsifiers have a subtle effect on the mucus that allows selective bacteria to penetrate and that causes inflammation and that causes a further change in the bacterial population.
- Mice consumption behavior changed based on quantity of emulsifiers consumed. Gerwirtz found that increased food consumption is driven by low grade inflammation. Mice consuming dextrin sodium sulfate (used to induce colitis) at low dose eat more. Researcher Rodger Kahn, Boston, showed that if the mouse is made insulin resistant in the brain they’ll eat more and develop similar phenotype. The conclusion is that low grade inflammation adversely impacts satiety sensation. Gary Wu, University of Pennsylvania has a clinical center set up for human eating design study. The main problem is how to get folks on an emulsifier free diet. They are now testing reactivity of lecithin (which is a more natural emulsifier). Lecithin may be used in the study if found to be without activity. They are also considering the possibility of having the cohort consume non-processed foods, but that introduces other variables.
- The emulsifier levels tested in mice are physiologically similar to what humans eat. For CMC, Gerwirtz found gut impact at 0 .5 percent but it is approved up to 2 percent for human food P80 caused gut impact in mice at 0.1 percent yet it is approved at 1 percent for humans. This is a decent approximation of someone eating a lot of processed food as well as the total load of the many emulsifiers contained in individual processed food products which are all additive.
- At 32.33 Does Gerwirtz now eat differently? Is Gerwirtz re-thinking his personal diet? Artificial sweetener studies are associated with inflammatory diseases. Dr. Gewirtz has changed his and his families diet. He does simple label reading for polysorbate 60 and 80, anything with “gum”. Did he realize any N=1 personal physiological changes eliminating these additives? Gerwirtz did not for himself, but they gradually eliminated the additives so they probably wouldn’t notice change. Emulsifier free ice cream does get freezer burn and it’s a trade off he is willing to take, Gerwirtz and his family now eats much less processed foods.
- Does the food industry need changed in how additives are tested? Yes, a major change in the food system is needed. Most additives are GRAS (genuinely recognized as safe) and not tested at all. GRAS means the additive was in use at the time the FDA decided they’d issue guidelines and everything then in food, was automatically assumed to be safe and received GRAS approval. Polysorbate 80 was tested for acute toxicity and tumor genesis, and that testing showed some concerns. To avoid toxicity P80 quantity was limited to 0.1 percent. But the health problems that have so much in common are not associated with acute toxicity but rather chronic low grade inflammation and these issues affect genetically susceptible hosts. So give emulsifiers to mice genetically predisposed to having colitis (TLR5 knockout mice and IL-10 deficient mice), which is what Gerwirtz did, and they saw a marked significant increased incidence in colitis. Even the natural product additives that have been around could have lower threshold limits.
In summary: JUST DO YOUR GUT MICROBIOME A FAVOR; ELIMINATE EMULSIFIERS and STOP NUDGING THE MICROBIOME INFLAMMATORY CASCADE OCCURRING IN THE MUCOSAL LINING that looks like that ASSOCIATED WITH IBD and METABOLIC SYNDROME, and only time will tell, what other inflammatory diseases in those with predisposition.
In health through awareness,
♥ Last updated: November 3, 2017 at 16:17 pm
to stop URL links for the caution and scroll icons. Prior update Sept 29, 2016 added in the section discussing restaurant meals: I did not include chicken. Why? Most have non-SCD broth injection.
More discussion on how diet substrates impact the constituency and thus the resultant metabolites and function of the microbiome.
Diet does not only exert a direct influence on intestinal immune and epithelial cell functions, but also shapes the intestinal microbial community by generating a milieu that favors the growth and metabolic activity of specific bacteria. The microbiota has a crucial role in the development and maintenance of the host’s immune homeostasis.[27,28] …long-term dietary patterns dominated the overall composition of the ecosystem, and temporal community changes shifted back to preintervention patterns.[40,44] ...long-term dietary habits, or antibiotic interventions exert a great perturbation on the intestinal community, from which the ecosystem may not recover. When this resilience is lost, and detrimental long-term factors influence the intestinal ecosystem toward a less favorable composition, the microbiota stabilizes in a ‘dysbiotic’ state. …resilience of the microbiota is lost in acute IBD[48,49] [as well as other diseases having signature microbiome skew] (Fig. 3). As recently termed by Joël Doré and Hervé Blottière, ‘dysbiosis must be viewed as an alteration of symbiosis, which drives a detrimental distortion of microbe-host homeostasis’. At present, dysbiosis is characterized by loss of diversity, change in composition, increase in pathobionts or mere changes in its functional character (meaning changes in the metabolic capacity without major changes in the composition). [This is a great definition.] -Reciprocal Interaction of Diet and Microbiome in Inflammatory Bowel Diseases
Why might probiotics not work well for disease?
“Probably one of the reasons is because probiotics die in a hostile environment like one found in an IBD gut or somebody with disease: inflammation and [an] oxidized environment. They [probiotics] don’t really know how to compete with the native flora, so they don’t have the right colonization factors.” -Messages about diet and IBD need to change, says Canadian researcher That is the first time I’ve read this, and it is an interesting thought. I also am aware however that FDA regs prohibit strains that colonize in commercial probiotics. I talk more about this in the post, PRESERVE & RESTORE LOSS OF MICROBIOME DIVERSITY IS AGGRESSIVE PREVENTATIVE MEDICINE. We need to learn a lot more about ferment consumer gut health, and that is one reason I work to profile consumers for Dr. Rob Knight’s upcoming ferment studies.
A quick look at types of fats and gut impact
Realize the fat type implicated as most damaging, Omega-6 polyunsaturated fats, usually is in most all processed foods, and the double whammy: such usually also contains emulsifiers (and other junk additives). And, if you eat low or no fat, you are missing out on the protective responses in the intestine fat actually can provide when it’s the right fat. And for those thinking popping fish oil while still eating a high processed Omega-6 load diet mitigates the risk… you are only kidding yourself. While that might modulate the dysbiotic gut microbiome, the oxidation in the liver is still a major problem (at least in mice). There’s no way around it. You can’t exercise your way out of a bad diet; you’ve got to eat yourself out of disease. The relevant studies:
- Eating a high PUFA-6 diet of processed and prepared foods and supplementing with PUFA-3 does not stop the oxidation and aging in the liver though it may mitigate the gut dysbiosis. High-fat diets rich in n-6 PUFA cause dysbiosis, and induce weight gain and inflammation. Fish oil supplementation reversed these effects, but also resulted in oxidative stress. Since oxidative damage is a detrimental effect associated with ageing, eating diets rich in n-3 PUFA with high levels of n-6 PUFA, as is recommended to combat excess n-6 PUFA in present ‘Western’ diets, may exacerbate gastrointestinal disorders in a vulnerable aged population. –Diets rich in n-6 PUFA induce intestinal microbial dysbiosis in aged mice
A diet rich in olive oil… even though it’s high fat… found beneficial during colitis. When compared to the monounsaturated fat (olive oil) diet for those with IBDs, Gibson’s research showed that a diet high in polyunsaturated fats (found in many common supermarket products) was far inferior. “When [they] eat polyunsaturated fats, omega 6 polyunsaturated fats in particular… that diet turns out to be the worst. It’s very pro-inflammatory. It’s the worst for colitis patients.” [Again, it is a double whammy. Just to repeat, a diet high in the Omega-6 usually also contains the gut damaging emulsifiers discussed in this post]. Meanwhile, a diet with mostly saturated fats fell somewhere in the middle. -Messages about diet and IBD need to change, says Canadian researcher
The future for IBD (and likely any other disease having signature microbiome skew) will include microbiota change, and diet is one mode to effect such change.
In the bigger picture of how to treat IBDs through microbiota modulation, Gibson says personalized dietary interventions will undoubtedly play a role. This will mark a change in clinical practice, since currently specific dietary changes are not routinely recommended for IBD patients. In addition, though, different strategies will be used to change microbiota for the long term — an area where science has so far come up short. -Messages about diet and IBD need to change, says Canadian researcher
Diets are being looked at for disease remission either alone or in combination with therapy.
Diet in the pathogenesis and treatment of inflammatory bowel diseases explains: Researchers have learned much about the effects of diet on the mucosal immune system, epithelial function, and the intestinal microbiome; these findings could have significant practical implications. Controlled studies of patients receiving enteral nutrition and observations made from patients on exclusion diets have shown that components of whole foods can have deleterious effects for patients with IBD. [NOTE: I have not read the entire article and do not know what components of “whole food” they consider to be deleterious. When I get the full text of this paper I’ll update]. Additionally, studies in animal models suggested that certain nutrients can reduce intestinal inflammation. In the future, engineered diets that restrict deleterious components but supplement beneficial nutrients could be used to modify the luminal intestinal environment of patients with IBD; these might be used alone or in combination with immunosuppressive agents, or as salvage therapy for patients who do not respond or lose responsiveness to medical therapies. Stricter diets might be required to induce remission, and more sustainable exclusion diets could be used to maintain long-term remission. [This is sounding like what Stanford is proposing in the Stanford 2016 study that found that liberalized SCD after strict adherence maintained remission for IBD].