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Fatigue after bowel movement

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I sometimes get extreme fatigue after a bowel movement (BM), so much so I have to lie down afterwards, my muscles are weak, I can't think or seem to function normally. Other than sometimes getting fatigue afterward I have to say that there is nothing abnormal about my BM's.
Does anyone know what this is or why it happens?
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First Helper Raeve
Users who thank Raeve for this post: chrisscott 

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replied October 13th, 2009
Extremely eHealthy
Extreme fatigue or feeling like fainting after bowel movement happens due to stimulation of vagus nerve, which supplies the neck, chest, and intestine.
When stimulated, the vagus nerve slows the heart, decreases its pumping function resulting in reduced blood flow to every body part, including brain.
If you strain to pass a stool, straining will contribute to experience the same symptoms, since straining reduces the amount of blood flowing back to the heart.

If this happens after exercises and other activities with exertion, consult a cardiologist!
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replied March 24th, 2016
So, what are you supposed to do to prevent this from happening? I get so weak after a bowel movement that I sleep for 1-2hrs some times. Is there something that can be done before or after to get the blood back to the heart. An herb? supplement? anything????
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replied May 28th, 2010
extreme fatigue after bowel mvt
I had had extreme fatigue after bowel mvt for years, finally I was diagnosed having the parasite D.fragilis.
Read the following article:


During the 5-year study period, 25 pediatric patients were diagnosed withD. fragilis infection, thereby identifying D. fragilis as a relatively rare parasitic cause of infectious diarrhea in our institution. Only 0.3% of all stool samples collected were positive for D. fragilis within the study period. In comparison, Giardia lamblia was identified in 2% of specimens sent for parasitologic study. Symptoms in 11 patients for whom clinical details were available varied from chronic, low-grade abdominal pain with diarrhea and vomiting, to severe, paroxysmal abdominal pain that required hospitalization. In our series, there were no complaints of fatigue, anorexia, or weight loss (11).The representative case had leukocytes identified in stool that were suggestive of colitis that ultimately was confirmed by colonoscopic examination. The patient was well for a period, eating a milk-free diet for her challenge-confirmed diagnosis of allergic (eosinophilic) colitis. However, the patient's diarrhea and abdominal pain later recurred, despite strict adherence to a bovine and soy protein-free diet. The moderate degree of colonic inflammation and extensive eosinophilic infiltrates noted on repeat colonoscopy were consistent with an allergic or parasitic etiology.

The patient's symptoms completely resolved once the D. fragilis was identified in microscopic stool examination and treated with iodoquinol.

Interestingly, results of a subsequent milk challenge were negative, and the child has subsequently tolerated milk products.The outcome in this case illustrates that infestation with D. fragilis may have a clinical picture indistinguishable from allergic colitis. There is a common tendency to label patients as milk-protein allergic, in view of the lack of a reliable diagnostic test(10). Awareness of this parasite as a possible cause of chronic diarrhea and eosinophilic colitis is thus important. Although colitis has been previously documented in one adult patient, there was no evidence of peripheral eosinophilia or eosinophilic infiltrates in biopsy specimens(9).The high prevalence of D. fragilis infestation seen among institutionalized people and in those with a history of foreign travel or recent immigration identifies risk factors(3,4,12,13). However, the pathogenicity of D. fragilis remains unclear. Keystone et al. showed that only 10% of institutionalized pediatric patients infested with D. fragilis had clinical symptoms (14). Among our 11 patients, only the one (Table 1) with the colonic juvenile polyp, was a carrier of D. fragilis. Conversely, patient 10(Table 2) remained symptomatic until the successful eradication of D. fragilis infestation.D. fragilis lacks a cyst stage, rendering laboratory detection difficult. However, virtually 100% accuracy in identifying D. fragilis can be achieved using the proper laboratory fixation and coloration techniques. Polyvinyl alcohol, sodium-acetic acid formula, or Scharedinn's fixative are the preferred preservatives(2,15). More recently, immunofluorescence has been used in an attempt to eliminate the need for visual identification(16). These preservation and staining techniques have improved the rate of D. fragilis recovery, allowing clinicians to associate this parasite with a variety of gastrointestinal symptoms(2,11).D. fragilis is thought to be transmitted either by the fecal-oral route, or in person-to-person contact. Because it has no cyst stage, contaminated food or water would seem an unlikely mode of transmission. Using isoelectric point determination, D. fragilis was identified inE. vermicularis eggs, thereby confirming the latter as a potential vector of transmission (17). E. vermicularis has also been associated with symptoms of abdominal pain, with eosinophilia independent of D. fragilis (11). E. vermicularis coinfection was not found in our series. However, stools in three patients were coinfected with B. hominis, the pathogenicity of which remains speculative.The generally recommended treatment for D. fragilis is iodoquinol(1Cool. The most effective therapy for dientamoebiasis was reported to be a pentavalent arsenical, diphetarsone. Although this drug was reported to be 95% effective in eradicating the infection(19), it is not widely available. Other drugs of choice are metronidazole, paromomycin, and tetracycline; the latter, however, is not used in children
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replied September 18th, 2015
This is a known syndrome, though docs are clueless about it. Here are two links that might be helpful:

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