They have already demonstrated PI IBS as a brain gut axis disorder.
This is one reason why not all people with an enteric infection develop IBS.
The CRF is anotheer issue with the brain and signals coming from the gut. The gut singals the brain and the brain realeases CRF and signals back to the gut. This is part of the HPA axis responce. It singals mast cells in the gut and they release histimine unto the smooth muscle and that contributes to the pain.
Readers' Exchange
Defining Stress in IBS
Fall 2003
From Arizona -- Thank you so much for your efforts and support for those of us with GI disorders. Your first issue (Spring 2003) of Digestive Health Matters is both professional and informative. I would like to comment on one of the articles - "The CNS: Center for Neurovisceral Sciences and Women's Health at UCLA." I am encouraged to know that steps are being taken for funding research of IBS and interstitial cystitis. However, it is discouraging that researchers are still expending time and money to research "neurobiological mechanisms by which stress modulates brain-visceral interaction." I realize that stress is a popular theory in the discussion of IBS triggers, however, I believe this is completely backward and it is the chronic pain and totally unreliable bowel function of an IBS sufferer which causes the greatest stress. If research would focus on "fixing" the bowel, no doubt the panic and fear of IBS would be greatly alleviated.
Comment from Emeran A. Mayer, M.D. -- In contrast to the common interpretation of the term "stress" as a psychological phenomenon, it should be understood as any real or perceived perturbation of an organism's homeostasis, or state of harmony or balance. For example, in this viewpoint a severe hemorrhage, starvation, extreme temperature, or worry about the unpredictable onset of abdominal pain all qualify as stressors -- some as "physical" stressors, others as "psychological" stressors. The fear to leave the house in the morning without knowing if one can make it to work without having to stop on the freeway because of an uncontrollable bowel movement, or the fear of experiencing uncontrollable abdominal discomfort during an important business meeting are sufficient stressors to activate the central stress system.
The central stress system involves the release of chemical stress mediators in the brain (such as corticotropin releasing factor), which in turn orchestrate an integrated autonomic, behavioral, neuroendocrine, and pain modulatory response. This biological response in turn will alter the way the brain and the viscera interact, and this altered brain-gut interaction can result in worsening of IBS symptoms. Thus, pain and discomfort, fear of these symptoms, activation of the stress response, and modulation of the brain-gut interactions by stress mediators are part of a vicious cycle which need to be interrupted to produce symptom relief.
The neurobiology of stress is not a theory, but a topic that can be studied in animal models, and one of the hottest topics in drug development for treatment of IBS (e.g., substance P antagonists, corticotropin releasing factor antagonists).
Merck Manual
"In this disorder, the digestive tract is especially sensitive to many stimuli. Stress, diet, drugs, hormones, or minor irritants may cause the digestive tract to contract abnormally, usually leading to diarrhea. Periods of constipation may occur between bouts of diarrhea. Irritable bowel syndrome affects women 3 times more often than men.
The brain has enormous control over the digestive system. Stress, anxiety, depression, fear, and virtually any strong emotion can lead to diarrhea, constipation, and other changes in bowel function and can further worsen a flare-up (bout or attack) of irritable bowel syndrome."
http://www.merck.com...129/ch129d.html
Dr Wood's comments for me
"Dr. Jack Wood, a renowned physiologist at The Ohio State University calls the ENS the little-brain-in-the-gut.
"Dear Shawn:
Sorry for the delayed reply to your question. I generally agree with Dr. Drosssman's response. A subgroup of individuals when they become sensitized to specific molecules in certain foods respond to ingestion of the molecules with symptoms of cramping abdominal pain, fecal urgency and explosive watery diarrhea. These are also the primary symptoms of diarrhea-predominant IBS. Enteric mast cells, by mechanisms we don't understand, become sensitized to the food molecule and respond to its presence by releasing a signal to the brain-in-the-gut (ENS) which is interpreted as a threat. The ENS responds by running a program which organizes secretion and motility into a behavior pattern of the bowel, which rapidly clears the threat from the lumen. Because to be effective secretion occurs in large volumes and the contractions that accomplish rapid propulsion are strong, running of the program has the side effects of diarrhea and cramping pain.
Big brain input to mast cells during stress activates the mast cells to evoke the symptoms resulting from exposure of the mast cells to sensitizing food antigens. Aside from food allergens and mast cells, certain chemicals such as those in hot peppers, stimulate sensory nerves in the ENS and we are beginning to understand how this can also lead to food-related symptoms that might mimic or exacerbate IBS.
Hope this helps,
Jackie (Jack) D. Wood "
FYI
"You have two brains: one in your head and another in your gut. Dr. Jackie D. Wood is a renowned physiologist at The Ohio State University. He calls the second brain, "the-little-brain-in-the-gut." This enteric nervous system is part of the autonomic nervous system and contains over one hundred million neurons, which is as many as are in the spinal cord. This complex network of nerves lines the walls of the digestive tract form the esophagus all the way down to the colon. This little brain in the gut is connected to the big brain by the vagus nerves, bundles of nerve fibers running from the GI tract to the head. All neurotransmitters, such as serotonin that are found in the brain are also present in the gut.
Dr Wood has discovered that this little-brain-in-the-gut has programs that are designed for our protection and which are very much like computer programs. They respond to perceived threats in the same way that the limbic system or the emotional brain does. So the threat of a gastrointestinal infection can activate the program that increases gut contractions in order to get rid of the infection. The symptoms are abdominal cramping and diarrhea.
Dr. Wood has determined that a type of cell found in the body and the gut, called the mast cell, is a key to understanding the connection of the big brain in the head with the little-brain-in-the-gut. Mast cells are involved in defense of the body. In response to certain threats or triggers, such as pollen or infection, mast cells release chemicals, such as histamine, that help to fight off the invader. Histamine is one of the chemicals that causes the symptoms of an allergy or a cold. When an infection of the gut occurs, such as food poisoning or gastroenteritis, the mast cells of the gut release histamine. The little-brain-in-the-gut interprets the mast cell signal of histamine release as a threat and calls up a protective program designed to remove the threat at the expense of symptoms: abdominal pain and diarrhea.
The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut. Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not. So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea."
So two majorally important cells in the gut are enterochromaffin cells and mast cells. The enterochromaffin cells or EC cells release serotonin to start gut contractions. This process helps explain d and c and d/c.
The alteration in the gut is seen as a "threat" by the brain and the brain's hpa axis is then activated.
These cells are embedded in the lining of the gut brain and are close to each other.
IN PI IBS they have found an increase of both these cells embedded in the gut.
"By using sophisticated imaging techniques that allow us to visualize the activity of the living human brain (see “Looking Into the Living Human Brain”), researchers at the UCLA Neuroenteric Disease Section have recently identified for the first time the regions within the brain that are involved in the perception and modulation of visceral sensations, including visceral pain. In addition, by comparing brain responses to an acute intestinal stimulus between healthy control subjects, patients suffering from IBS, and patients with ulcerative colitis, they were able to identify specific alterations in how the brains of IBS patients process and respond to acute colonic pain."
History of functional disorders.
MOTILITYIn healthy subjects, stress can increase motility in the esophagus, stomach, small and large intestine and colon. Abnormal motility can generate a variety of GI symptoms including vomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GI
patients have even greater increased motility in response to stressors in comparison to normal subjects. While abnormal motility plays a vital role in understanding many of the functional GI disorders and their symptoms, it is not sufficient to explain reports of chronic or recurrent abdominal pain.
VISCERAL HYPERSENSITIVITY Visceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain, which are not well correlated with changes in gastrointestinal motility, and in some cases, where
motility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lower pain threshold with balloon distension of the bowel or have increased sensitivity to even normal intestinal function. Additionally, there may be an increased or unusual area of somatic referral of visceral pain. Recently it has been concluded that visceral hypersensitivity may be induced in
response to rectal or colonic distension in normal subjects, and to a greater degree, in persons with IBS. Therefore, it is possible that the pain of functional GI disorders may relate to sensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injury to the viscera.
BRAIN-GUT AXIS
The concept of brain-gut interactions brings together observations relating to motility and visceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinal and CNS central nervous system activity, the brain-gut axis explains the symptoms relating to functional GI disorders. In other words, senses such as vision and smell, as well as enteroceptive information (i.e. emotion and thought) have the capability to affect gastrointestinal sensation,
motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect central
pain perception, mood, and behavior. For example, spontaneously induced contractions of the colon in rats leads to activation of the locus coeruleus in the pons, an area closely connected to pain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associated with a decrease in the frequency of MMC activity of the small bowel possibly mediated by stress hormones in the brain. Based on these observations, ccc it is no longer rational to try to discriminate whether physiological or psychological factors produce pain or other bowel symptoms. Instead, the Functional GI disorders are understood in terms of dysregulation of brain-gut function, and the task is to determine to what degree each is remediable. Therefore, a treatment approach
consistent with the concept of brain-gut dysfunction may focus on the neuropeptides and receptors that are present in both enteric and central nervous systems.
med.unc.edu/medicine/fgidc/historyfunctionaldisorders.pdf
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My website on IBS is www.ibshealth.com
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