BREAKING! Cornell Study Finds That Inulin Supplements Promoted For Weigh Loss Or As A Rich-Fiber Source Can Actually Induce Type 2 Inflammation!
: Researchers from Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Weill Cornell Medicine, Cornell University, New York – USA have found that the health supplement Inulin that is often promoted for weight loss or a rich-fiber source suitable for diabetic and those with high cholesterol and triglyceride levels or even a prebiotic can actually cause more serious health issues as it can actually induce type two inflammation.
Type 2 inflammation is a pattern of immune response. Its physiological function is to defend the body against helminths, but a dysregulation of the type 2 inflammatory response has been implicated in the pathophysiology of several diseases and can also be triggered via abnormalities in microbiota-derived metabolites.
In type 2 inflammation, IL-25, IL-33, and TSLP are alarmins released from damaged epithelial cells. These cytokines mediate the activation of type 2 T helper cells (Th2 cells), type 2 innate lymphoid cells (ILC2 cells), and dendritic cells. Th2 cells and ILC2 cells secrete IL-4, IL-5 and IL-13. IL-4 further drives CD4+ T cell differentiation towards the Th2 subtype and induces isotype switching to IgE in B cells. IL-4 and IL-13 stimulate trafficking of eosinophils to the site of inflammation, while IL-5 promotes both eosinophil trafficking and production.
Although dietary fibers can exert beneficial anti-inflammatory effects through microbially fermented short-chain fatty acid metabolites, the immunoregulatory roles of most fiber diets and their microbiota-derived metabolites remain poorly defined.
The study team utilizing microbial sequencing and untargeted metabolomics showed that a diet of inulin fiber alters the composition of the mouse microbiota and the levels of microbiota-derived metabolites, notably bile acids.
Alarmingly, this metabolomic shift is associated with type 2 inflammation in the intestine and lungs, characterized by IL-33 production, activation of group 2 innate lymphoid cells and eosinophilia. Delivery of cholic acid mimics inulin-induced type 2 inflammation, whereas deletion of the bile acid receptor farnesoid X receptor diminishes the effects of inulin.
The effects of inulin are microbiota dependent and were reproduced in mice colonized with human-derived microbiota.
It was found that genetic deletion of a bile-acid-metabolizing enzyme in one bacterial species abolishes the ability of inulin to trigger type 2 inflammation.
The study findings demonstrated that inulin enhances allergen- and helminth-induced type 2 inflammation.
The study data reveal that dietary inulin fiber triggers microbiota-derived cholic acid and type 2 inflammation at barrier surfaces with implications for understanding the pathophysiology of allergic inflammation, tissue protection and host defense.
The study findings were published in the peer reviewed journal: Nature.
Ironically, inulin dietary fiber supplements have been promoted as health supplements
n> for a long time with claimed anti-inflammatory properties, unknown to many that it is actually causing an allergy-related type of inflammation in the lung and gut, and other parts of the body!
It should also be noted that certain processed foods also use Inulin as a sweetener in certain products.
The study is the first to find that dietary inulin fiber alters the metabolism of certain gut bacteria, which in turn triggers what medical researchers’ term as type 2 inflammation in the gut and lungs.
Such type of inflammation is thought to have evolved in mammals chiefly to defend against parasitic worm ("helminth") infections, and is also part of normal wound-healing, although its inappropriate activation underlies allergies, asthma and other inflammatory diseases.
Co-Senior Author, Dr David Artis, Director, Friedman Center for Nutrition and Inflammation and the Michael Kors Professor of Immunology at Weill Cornell Medicine told Thailand Medical News, “There's a lot to think about here, but, in general, these findings broaden our understanding of the relationship between diet, immunity, and the normally beneficial microorganisms that constitute our microbiota and colonize our bodies."
The research team reflect the Friedman Center's highly cross-collaborative research mission, drawing on expertise in bacterial genetics, biochemistry and immunology at Weill Cornell Medicine in New York City and Cornell's Ithaca campus.
Assistant professor of immunology in medicine at Weill Cornell Medicine-Dr Chun-Jun Guo, and professor at the Boyce Thompson Institute and in the Department of Chemistry and Chemical Biology in the College of Arts and Sciences on Cornell's Ithaca campus-Dr Frank Schroeder teamed up with the Artis laboratory to gain a detailed understanding of how an important dietary component affects the microbiome and the immune response.
Dr Mohammad Arifuzzaman, a postdoctoral researcher in the Artis laboratory is the study's first author and is also director of the Jill Roberts Institute for Inflammatory Bowel Disease at Weill Cornell Medicine.
It should be noted that small amounts of inulin are present in a wide variety of fruits and vegetables, including bananas, asparagus, and garlic besides being concentrated in commonly available high-fiber dietary supplements.
Past studies misleadingly claimed that inulin boosts populations of beneficial gut bacterial species which in turn boost levels of anti-inflammatory immune cells called regulatory T (Treg) cells.
This new Cornell study examined inulin's effects more comprehensively.
The study team gave mice an inulin-based, high-fiber diet for two weeks, and then analyzed the many differences between these mice and mice that had been fed a diet lacking inulin.
It was found that the inulin diet, while increasing Treg cells, also induced markedly higher levels of white blood cells called eosinophils in the gut and lungs. A high level of eosinophils is a classic sign of type 2 inflammation and is typically seen in the setting of seasonal allergies and asthma.
The study team also found that the eosinophil response was mediated by immune cells called group 2 innate lymphoid cells (ILC2s), which were activated by elevated levels of small molecules called bile acids in the blood. The bile acid levels were elevated due to the inulin-induced growth of certain bacterial species-group called Bacteroidetes, found in both mice and humans which have a bile acid-metabolizing enzyme.
Dr Schroeder said "Our study team was amazed to find such a strong association between inulin supplementation and increased bile acid levels. We then found that deletion of the bile acid receptor abrogates the inulin-induced inflammation, suggesting that microbiota-driven changes in bile acid metabolism underlie the effects of inulin."
Dr Guo added, "When we colonized germ-free mice (mice without microbiota) with one of these bacterial species, and then knocked out the gene for one bacterial enzyme that promotes bile acid production, the whole pathway leading from inulin to eosinophilia and allergic inflammation was blocked."
The study team also found that inulin did worsen allergen-induced type 2 airway inflammation in mice.
It should be noted that type 2 inflammation has been implicated in several chronic diseases including Asthma, Atopic dermatitis, Chronic sinusitis with nasal polyps and Eosinophilic esophagitis.
Importantly persons with one type 2 inflammatory disease are more likely to have other type 2 inflammatory diseases. https://erj.ersjournals.com/content/56/suppl_64/232
Over time, chronic inflammation can trigger your immune system to attack healthy tissue and organs in your body. When left untreated, prolonged chronic inflammation can increase your risk for diseases like diabetes, heart disease, cancer and rheumatoid arthritis.
The study team now plan to use their multi-disciplinary, multi-platform approach to study systematically the immune effects of the different types of dietary fiber as well as a range of other dietary supplements in different states of health and disease.
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