a tea of ingredients known to clam/sooth and/or to be anti-inflammatory helped. This is not a big surprise. (I am also very glad to hear it helped you personally. Thanks for sharing.) I drink a turmeric-ginger tea almost daily.
Many other plant extracts (like compounds found in the bark of Willow trees) are the basis of some of today's most successful drugs for managing IBD (i.e., 5-asa).
BTW, if you have to keep drinking the tea it is technically not a "cure" but a "management". A cure would reset the epigenetic changes associated with the autoimmune response and/or re-balance the gut microbiota, and bring one back to original condition. But I realize this is hair splitting.
The nutritional modulation of IBD is getting increased attention. nutritional conditions that make triggering the disease easier, nutritional conditions that might block/promote inflammation, nutritional conditions that regulate the immune system, and nutritional conditions that regulate the gut microbiota. There are a growing number of research articles on this and new lines of research developing. Some of it beginning because of anecdotal reports like this tea, and some because of studies with ancient herbal tonics.
Nutritional Modulation of the Inflammatory Bowel Response. Ioannidis, O., et al. (2011). Digestion 84(2): 89-101. said...
Crohn's disease and ulcerative colitis represent distinct phenotypic forms of inflammatory bowel disease and continue to be a common cause of morbidity. The corticosteroids and the immunomodulatory drugs, which are the basis of treatment for the inflammatory bowel diseases, do not assure always satisfactory outcomes. Nutrition has been used in order to modify the inflammatory response of various chronic inflammatory diseases, including Crohn's disease and ulcerative colitis. In the pathogenesis of inflammatory bowel diseases, the intestinal microflora and the intestinal mucosal disorders play a crucial role. Also, the release of reactive oxygen species is a significant factor of initiation and preservation of the inflammatory reaction in these diseases. The advantages of the nutritional treatment derive from the sequestration of intraluminal agents which may promote the inflammatory bowel response or, alternatively, nutrition is able to modify the immune response, reducing the uncontrolled inflammatory reaction. Furthermore, nutrition can enhance the mucosal barrier function and consists a significant source of antioxidants. This review focuses on certain nutritional components that modulate the inflammatory response of the bowel and aims to present a rational thesis regarding the use of nutritional agents in the management of inflammatory bowel diseases. Copyright (C) 2011 S. Karger AG, Basel
Quincy will have to speak to her concerns about
food/diet threads, but I have my own concerns even though I understand all the potential of nutritional approaches. My concerns group into two main areas:
1) often the diets are fads that are not connected to the growing "nutritional modulation" literature
2) people make the assumption that diet is a causal agent and further that it would also be a curative agent. (modulation is far form cure). In a way this is like thinking that since clockwise spinning blades on a lawnmower shortened grass, that counter-clockwise spinning blades would make it grow. Key questions are if "damage" has been done that will persist if the trigger is removed?, and whether the epigenetic/microbiome lock is like an ordinary lock/key? For an ordinary lock, the same key locks and unlocks. But there are plenty of systems where a different key is needed to unlock. So something that triggered an undesirable change in a person's epigenetic settings or microbiome, is not necessarily the same thing that can change it back.
Personally, I think it is the "stupid" diet people, and the for-profit diet fad industry, that has made a lot of doctors reluctant to acknowledge diet with patients. In short, it can let in a lot more stupid than useful. However, ultimately, they cannot ignore the growing research.
Some other good reads are:
Gentschew, L. and L. R. Ferguson (2012). Role of nutrition and microbiota in susceptibility to inflammatory bowel diseases. Molecular Nutrition & Food Research 56(4): 524-535. said...
Inflammatory bowel diseases (IBDs), Crohn's disease (CD), and ulcerative colitis (UC) are chronic inflammatory conditions, which are increasing in incidence, prevalence, and severity, in many countries. While there is genetic susceptibility to IBD, the probability of disease development is modified by diet, lifestyle, and endogenous factors, including the gut microbiota. For example, high intakes of mono- and disaccharides, and total fats consistently increases the risk developing both forms of IBD. High vegetable intake reduces the risk of UC, whereas increased fruit and/or dietary fiber intake appears protective against CD. Low levels of certain micronutrients, especially vitamin D, may increase the risk of both diseases. Dietary patterns may be even more important to disease susceptibility than the levels of individual foods or nutrients. Various dietary regimes may modify disease symptoms, in part through their actions on the host microbiota. Both probiotics and prebiotics may modulate the microflora, and reduce the likelihood of IBD regression. However, other dietary factors affect the microbiota in different ways. Distinguishing cause from effect, and characterizing the relative roles of human and microbial genes, diet, age of onset, gender, life style, smoking history, ethnic background, environmental exposures, and medications, will require innovative and internationally integrated approaches.
... and:
Forbes, A., et al. (2011). Nutrition in Inflammatory Bowel Disease. Journal of Parenteral and Enteral Nutrition 35(5): 571-580. said...
The diet of industrialized nations may contribute to the pathogenesis of both ulcerative colitis (UC) and Crohn disease (CD). Malnutrition is relatively unusual in UC, but in CD, which often affects the small intestine, it is frequent and may be severe. Nutrition support is therefore frequently indicated. First principles of artificial nutrition can be applied effectively using the gut whenever possible. Parenteral nutrition is generally required only in those with short bowel syndrome. An increasing literature (especially in pediatrics) favors the use of defined exclusive enteral nutrition (EN) in the primary treatment of active CD. Controlled trials are, however, lacking, and recommendations are accordingly not of the highest rank. It appears that in this context, simple polymeric regimens are usually sufficient, and there is currently insufficient evidence to make a strong recommendation for disease-specific feeds. In the maintenance of remission in CD, controlled data demonstrate that defined EN reduces the risk of relapse requiring steroid treatment. There are no data in support of primary nutrition therapy in UC either in management of the acute flare or in maintenance. In conclusion, nutrition therapy in adults with inflammatory bowel disease is probably both undervalued and underused, but the evidence base needs to be strengthened to confirm its efficacy, determine better those patients most likely to benefit, and optimize the regimens to be employed. (JPEN J Parenter Enteral Nutr. 2011; 35: 571-580)
Post Edited (DBwithUC) : 3/7/2013 10:13:58 AM (GMT-7)