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While reading posts on this BB, I've seen many lists of bad/good foods for people with IBS. However, it seems that while some foods may be bad for one person, they might be fine for another.Are there foods that are always good and safe? How about some that are always bad? Can we make some lists?[This message has been edited by jszobody (edited 05-22-2001).]
 

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You are right in that it depends on the person. For me, good foods include plain white rice,plain chicken,turkey,steak,baked potatoes, and eggs (usually hard cooked or fried with Pam),dry toast. Bad foods too many to list but the worst by far always are
izza, any fast foods like McD's and B.K.,any greasy foods, many or most kinds of fruit if too many are eaten, many veggies like broccoli or corn, blue cheese does me in for some reason, wine. Also, overeating of anything will send me running. I find that if I eat just one of something like 1 small slice of pizza I'm usually OK. If I go for a second, it's a guaranteed D experience.I've had this condition for 24 years and I haven't figured it out as of yet.
 

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Here are a couple of post with some commonly bad foods http://www.ibsgroup.org/ubb/Forum1/HTML/016516.html http://www.ibsgroup.org/ubb/Forum1/HTML/016514.html BRAT diet foods are generally safe (but something on the list will probably bother someone) It is a commonly used diet for starting to eat solid food after a GI bug kinda diet so tends to be well tolerated.Bannanas (do not eat if you've got a latex allergy).Rice (unless you are allergic to rice--which of the grains is rarer than wheat or corn, but still happens in some people).Applesauce Toast (but not if your Celiac or have problems with wheat or other gluten problems).One on common dietary causes of gas and the other on common dietary causes of diarrheaK.------------------I have no financial, academic, or any other stake in any commercial product mentioned by me.My story and what worked for me in greatly easing my IBS: http://www.ibsgroup.org/ubb/Forum17/HTML/000015.html [This message has been edited by kmottus (edited 05-22-2001).]
 

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The only guaranteed safe Foods (no possible "reaction") I can think of are:watersaltEvery other type of food is potentially reactive in one way or another through one or more mechanisms. There is no 100% safe food for everyone, except the above (and then only when taken in appropriate amounts. Even water and salt can cause problems if overconsumed I should point out before someone else does!)Drink upMNL__________ www.leapallergy.com
 

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I believe as I get older and I mean old, we can become alergic to certain foods that we could eat without a bad reaction. For example; my mom has now becomed alergic to fresh tomatoes. She became alergic a few years ago to chocolate. A few years later I also became alergic to chocolate. So, look towards your parents, siblings, relatives, for their alergys, I think it's in the genes, DNA.I have become alergic to corn and my new grandchild is also alergic to corn. I get ibs-d.My mom has ibs-d.
 

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Hi EricNice pictures quantifying a phsyiologic response to various hormones and neurochemical mediators which regulate tone and contractile patterns. But it does not make the vital point. In fact admiring the detection of hypercontractility is interesting, but it can distract from the next and more important element: discussing the actual mechanisms, and then the possible underlying causes.As in asthma, for example, we can chart and illustrate all day long the hypercontractility of the bronchial smooth muscle with all manner of detection methods of the phenomenon. But at the end of the day one must answer the question as to the origin. So one must understand mast cells and chemical mediators released from mast cells and their effects on the nerves and smooth muscle of the bronchi as well as the CNS if and when they enter the systemic circulationThe small bowel (and even the large bowel) function very much like the bronchi in that regard.Nobody working on the symptoms sets associated with IBS and investigating them (from either the symptomatic diagnostic approach nor the causal approach) disputes that in IBS there is an exaggerated set of contractile responses. That would be akin to arguing from what direction the sun rises.(Res Ipsa Loquitur.)In fact, nobody disputed it 30 years ago when it was "spastic colon" or whatever you wanted to call it. We can just more easily quantify the neurochemical and neuromusculur actions with current technology.But the quantification of the phenomenon itself is no more revealing than going one step further and describing the discoorinated smooth muscle contractions seen in C types or the evacuatory contractions seen in d-types (an oversimplification). That is nothing more than a manifestion of an action-response.The smooth muscle itself is upregulated as are the sensory and motor nerves. The upregulation is not idiopathic. And it is not an idiopathic disease, it is a neuromuscular manifestation of a chemical process which in various forms elicits specific signs and symptoms clinically.The question that must be addressed is WHY. In fact, all the chemical mediators and hormones which upregulate all the structures along the brain-gut axis and within the gut itself and all its many structures are well known. Their sources are well known, and investigators are finding these substances (or markers therof) in reactive bowels. It has been going on (quantifying them) for over 25 years, since the first time prostaglandin E2 was found to be elevated in the feces of IBS patients and not in the controls. Or that IBS patients often responded to immunomodulating drugs. A red flag is a red flag.The mucosal immune response and the mediators released are implicated, as is the cellular immune response within the microvasculature of the samll bowel and then (as a consequence of circulating the chemicals via plasma, and ongoing cellular response) systemically. Leukotrienes, cytokines, serotonin, histamine, jeez, up to 100 different chemical mediators which have direct effects on the involved anatomy have been seen in the plasma, in the gut wall, in the vicinity of the neuroganglia in the gut wall. Even the very cell-types that release the chemicals can be seen aggregating in some cases in the vicinity of the gut wall neuroganglia. What does one suppose the consequence is and what elicited this action?The fluids withdrawn from the small bowel when it is challenged by specific ingestants confirmed to cause bowel distress on oral challenge point a very large arrow at WHY this upregulation is seen. The known actions of delayed-mechanisms of cellular response are highly suspicious in the subpopulation where the specific food response is seemingly inscrutable ("no food involvement" should probably read "not discernible by conventional means").This information is often not considered, but to do so is to set aside a large causal piece of the puzzle. This should not be done. The data must be integrated to get the full picture.To state "there is an exaggerated contractile response itself" is incomplete. It describes the consequence of something unmentioned. It cannot happen by itself. There must be an etiologic basis for this physiologic action.So it is either neurochemical or it is specific lesion-induced hypercontractility or it is both. And then what is the basis for the aberrant response itself? Is it dysfunction of elements of an immune response, or has the immune reponse been altered so as to produce this effect? If altered what is the basis of the altered response? Unseen pathogenic activity and endo or exotoxin effects on cellular response? Loss of adaptive functions secondary to enzymatic detoxification deficiency or dysfunction? There are many pathways which can lead to an end-point of observable upregulation of any neuromuscular structure, esp. in IBS.What is known is, as you illustrate, that it occurs. What is also known is the chemicals have been seen and implicated. Things which elicit their release can be quantified. As yet no syndrome-specific "lesion" has been quanitifed, but the aberrant mucosal and cellular responses have. And it is also pretty obvious that the colon is not the shock organ in IBS, it appears to be an affected organ systemically (except at the ileocecal junction, where increased mast cell tissue density is seen suggesting a site of chronic insult which elicits mast-cell concentration at that site). The site of primary insult seems very much to be the small bowel, almost regardless of which subpopulation is examined.To learn about the mediators implicated by the work of those doing direct jejunal isolation and in vitro analysis of cellular response, this is a good general text "THE IMMUNE SYSTEM" by Peter Parham. http://www.amazon.com/exec/obidos/ASIN/081...76326/sr=2-3/re f=sc_b_3/107-4326764-6290107[/URL] At least there is a summary in one place of all the basice mechanisms and the primary chemical mediators produced by various immune and non-immun but cell-targted reactions, and Brostoffs latest book on the whole spectrum of food intolerance and allergy can tie-out their physiologic effects in response to ingestants. http://www.amazon.com/exec/obidos/ASIN/072...r=2-2/102-64875 08-3420903[/URL] Eat well. Think well. Be well.MNL____________________ www.leapallergy.com [This message has been edited by Mike NoLomotil (edited 05-23-2001).]
 
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