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Frangible
I've had IBS-type symptoms (multiple food sensitivities in skin prick testing) and diarrhea/gas/bloating that was significantly worse when I was younger, but are still somewhat with me today. And I find that when I'm symptomatic with those things, my anxiety / discomfort levels increase, and my desire to leave the house, hit the gym, socialize, etc take a downturn. Not surprising.

I guess at some point I tuned it out and tried ignoring it. But the effects are there nonetheless. I think it's something that's worth paying attention to, though.

Random anecdotes...

For about a solid year, I was eating Kashi GoLean cereal in the morning. In terms of a nutrition profile, it's awesome stuff. But it killed my gut-- I had horrible gas, bloating, and frequent trips to the bathroom for half the day. I blamed the effects on my dexedrine, but they were there without it nonetheless. Switching over to Muscle Milk (premixed protein drink) keeps my gut solid and quiet. The sugar-alcohol sweetened protein bars also just killed me.

Another random anecdote...

My parents enjoy eating at a local asian diner, and so I ate dinner at the same place with them on and off for years. A while back, they switched teas to some Lipton carribean(?) blend, actually a very common tea blend. However, I had a severe allergic reaction to the tea, and it caused my throat to constrict and it was, obviously, a traumatic experience. However I didn't know it was the tea-- the first time I assumed I wasn't chewing well or something. The second, I thought it might be the soy sauce on the food. But it wasn't. The third, I forgot to order tea, so I got water, and was OK. The fourth, I had the tea again, and the fifth, I finally realized what was going on.

So, I've noticed that the food there gives me IBS-type symptoms, which is odd since I order teriyaki chicken and it is actually prepared very well; lean grilled chicken, brown rice, and some pretty simple soy sauce. I have no sensitivity in testing to either rice or chicken, and rice is the only grain (afaik) that doesn't ferment in the gut. One would think getting gas/bloating/diarrhea from such a dish would be puzzling. I could find no logical reason why the food itself would bother me, and so I assumed it was psychological.

Just in case though, the last time I ate there, I brought alone some simethicone (Gas-X) and random hippie digestive enzyme supplement. And I noticed something very strange.

I had little anxiety and was in a good mood, and was just fine drinking my water before the meal. But when the food came, before I could even swallow the first bite, I felt spasming of what I assume is my colon. Again, no psychological anxiety or stress I could perceive. I did some fourfold breaths, focused on my hara / fire chakra in that area, etc and nonetheless it did not stop. I ate the meal anyway, and figured it would be at worse like it was last time... some moderate gas/bloating that might be attenuated by the simethicone or enzymes.

But the next day my colon was still spasming. And the next. And the next. And the two days I took off from work. And the weekend. Only after days of loperamide and eating very carefully did it go back to normal.

And in that time, my ab muscles cramped up, my posture is worsened (and the muscles are still tender when I stretch), and my lumbar-area muscles contracted sympathetically to mirror the ventral ones.

My past history of health problems has been characterized by knee pain that is directly linked to hip muscle tension and over contraction. I always assumed this was due to flexibility problems and weakened muscles elsewhere (ie, VMO)... but after seeing what the fallout from that single meal did to my muscle tone in the area and knee pain symptoms from that, I wonder... could gastrointestinal problems also not play a role?

And further... why did it seem so psychologically driven (before I had even swallowed the first bite) , even though my anxiety/stress/mood were all fine? Can the enteric nervous system have some sort of "panic" reaction outside the CNS, or without obvious manifestations in the CNS? I'm grasping at straws here, but it just seemed like such an odd reaction that was removed from my mental state.
graatch
i'm kind of sleep deprived ... i can definitely chip in. do you remember my nervous spasm stomach problem?

straight up, to not delve into the matter too much right now, for rapid attenuation of the problem the best thing i found for it is spinach and massive doses of DGL

unfortunately, this is going to be in the relam of theory, outside of the DSM-IV tongue.gif
SoulSeeker
This is speculative, but we're grasping at straws anyway:

It sounds like you developed some sort of a conditioned response to eating that food. Not a pure conditioned response, since it seems like you haven't gotten the spasms before, just the severe allergic reactions. But your mind/body probably associated eating food at the Chinese diner with becoming ill, and reacted in a way to protect yourself from eating it again.

Even though you might not have felt very anxious, it's clear you knew at the time that there was a possibility of it happening again (i.e. the Gas-X & OTC hippie). Thus, on a subconscious level, your mind/body recognized the threat, and probably mobilized you into spasms so as to not even risk getting severe allergic reaction again. The spasms probably kept up either to reinforce that lesson, or because the feedback loop didn't get shut off properly. So just listen to your body, and quit eating at the diner.

I know it sounds far-fetched, but the mind/body connection can be extraordinarily powerful. I have heard of studies involving the placebo effects where they expose allergic people to a neutral plant they're not allergic to (but tell them they're allergic to it), and they break out in an allergic reaction because they believe they will. Similarly, when some pregnant women were given ipecac (which induces vomiting) and told it was morning sickness medicine, it actually reduced their nausea.

Psychosomatic phenomena can be powerful, especially when it comes to ingesting food, because we've evolved to avoid poisoning ourselves. I knew a college professor that had a bad flu one morning when eating Captain Crunch. It just took one-trial learning to subconsciously associate that cereal with feeling nauseating. He can't even look at a box of it without feeling sick again.
FunkOdyssey
QUOTE
So, I've noticed that the food there gives me IBS-type symptoms, which is odd since I order teriyaki chicken and it is actually prepared very well; lean grilled chicken, brown rice, and some pretty simple soy sauce.


I'll throw out wheat/gluten/soy (all of these are in soy sauce) sensitivity/intolerance/allergy as possible real biochemical causes.
ozzman
I know that feeling...sometimes random, sometimes just the thought of not being close to a bathroom, sent me in a panic.

Two or three times a week. I was convinced it was the olive oil.

Enter probiotics ...knights in shining armor, came to rescue my girlie delicate stomach.

Don't discount the role of serotonin in the gut, as 5-ht4 acts on gastrointestinal motility...maybe add some propanolol:

******

J Clin Pharmacol. 1977 Jul;17(7):431-40.Click here to read Links
The "spastic colon" syndrome: therapeutic and pathophysiologic considerations.
Lechin F, Van Der Dijs B, Bentolila A, Peña F.

Low doses of d-amphetamine plus propranolol rapidly improved the abdominal pain in 165 "spastic colon" patients. Concomitantly, these drugs reduced the sigmoidal hypertonicity and the rectal inhibition found in the manometric studies performed in some of those patients. The sigmoidal tone and phasic activity were also decreased by anticholinergic drugs. These results suggest that a cholinergic-serotonergic hyperactivity of the myenteric plexus may be responsible for the "spastic colon" syndrome.

PMID: 328541
avantgarde
Any recs on a good probiotic ?

FunkOdyssey
The most effective probiotic I have used so far is trader joes and lifeway kefir (I think they are both made by lifeway because trader joes has the same exact ingredients, bacterial strains, and nutritional info and they come in the same bottle). I previously tried various brands of acidophilus & bifidus, theralac, custom probiotics, Align (bifantis), Activia yogurt, and many more. While I noticed various short-term benefits from some of them I have only had any enduring success with kefir for IBS-type symptoms.

It won't inflate any supplement vendor's profits but sometimes functional food comes out on top.
ozzman
I have had great results from Gut Health (by RPN), but have also used PV-8 (Nutrition Now).

And probiotic use is not an everyday thing...prebiotic should be...those little critters need stuff to eat. It seems I use a probiotic every 3-4 months for a month or so
Frangible
QUOTE
It sounds like you developed some sort of a conditioned response to eating that food. Not a pure conditioned response, since it seems like you haven't gotten the spasms before, just the severe allergic reactions. But your mind/body probably associated eating food at the Chinese diner with becoming ill, and reacted in a way to protect yourself from eating it again.


Yeah, I think so as well... from my body's standpoint nearly choking to death several times is a pretty traumatic basic survival issue. I always assumed though that such a reaction would make me feel significant psychological anxiety, arousal, and distress, but it did not. Maybe my assumptions were just wrong.

QUOTE
So just listen to your body, and quit eating at the diner.


Indeed. Though one would think it should be possible to override this kind of response-- but since I was relatively calm to begin with, I'm not sure that say, meditation would do much. Perhaps eating the food outside the context of the restaurant, or eating different food inside the restaurant, multiple times might help.

QUOTE
the best thing i found for it is spinach and massive doses of DGL


DGL?

QUOTE
I'll throw out wheat/gluten/soy (all of these are in soy sauce) sensitivity/intolerance/allergy as possible real biochemical causes.


In the past allergy testing I did have an allergy to soy, but not gluten. Yet I have consumed significant quantities of soy products (other than the Kashi cereal) with few ill effects. Actually I think rice is gluten-free anyway?

I'll grant you I might have a lesser sensitivity to soy at this point, but one would think that would take several minutes after consumption of the food to have an effect.

QUOTE (ozzman @ Apr 16 2008, 08:09 AM) *
I know that feeling...sometimes random, sometimes just the thought of not being close to a bathroom, sent me in a panic.

Two or three times a week. I was convinced it was the olive oil.

Enter probiotics ...knights in shining armor, came to rescue my girlie delicate stomach.


I've had them in the past, but I guess restocking my intestinal flora after this last episode wouldn't be a bad idea. Nonetheless, there are some psychological components going on here I'm not sure they can effect much, unless they have a direct role in colonic spasmicity / tone.

QUOTE
Don't discount the role of serotonin in the gut, as 5-ht4 acts on gastrointestinal motility...maybe add some propanolol:

******

J Clin Pharmacol. 1977 Jul;17(7):431-40.Click here to read Links
The "spastic colon" syndrome: therapeutic and pathophysiologic considerations.
Lechin F, Van Der Dijs B, Bentolila A, Peña F.

Low doses of d-amphetamine plus propranolol rapidly improved the abdominal pain in 165 "spastic colon" patients. Concomitantly, these drugs reduced the sigmoidal hypertonicity and the rectal inhibition found in the manometric studies performed in some of those patients. The sigmoidal tone and phasic activity were also decreased by anticholinergic drugs. These results suggest that a cholinergic-serotonergic hyperactivity of the myenteric plexus may be responsible for the "spastic colon" syndrome.

PMID: 328541


I thought d-amp had minor effects in effecting ACh release, that seems odd... all I can see d-amp doing is decreasing central nocicpetion? I could be wrong. Why would propanolol have an effect? My understanding is adrenoceptors aren't involved.

I know serotonin can make things worse, but there aren't any selective 5-HT4 antagonists aside from research drugs. ACh is a possibility... but eh... honestly the side effects of anticholinergics are worse imo than those of loperamide.

Loperamide definitely decreased the spasmicity for me. Bismuth sacyliate(sp) seemed to decrease pain/tension, possibly from inflammation there.
FunkOdyssey
DGL = De-Glycyrrhizinated Licorice (good luck spelling that without internet access), it removes the "active" component of licorice that inhibits cortisol metabolism and produces symptoms of excess aldosterone: water retention, high blood pressure, etc.

There's no gluten in rice, I was talking about the soy sauce. However if I had read your post more carefully I would have seen that your colon spasm began before eating the meal which invalidates my suggestion (although gluten intolerance is more often a matter of degree than is commonly realized -- its not much good for anyone).

I think probiotics in one form or another are definitely a good idea and I have no doubt that they can influence colonic spasticity. Pubmed'ing "spastic colon probiotics" returns 118 matches.
Concentrate
not exactly scientific, but there are 4 user reports on revolutionhealth of people using 5-htp for IBS with very good results. Its a super cheap supp so it might be worth a shot

http://www.revolutionhealth.com/drugs-trea...-diarrhea-ibs-d
graatch
Strange if 5-htp is helpful, as I would expect it to maybe worsen inflammation.

One thing I found that would (still does, I still have this problem, but not nearly as much -- except when*) really cause it to flare up is ... sugar alcohols, especially xylitol and inositol. Maltitol and sorbitol do it too, but for some reason xylitol is the worst. That's strange since xylitol iirc is supposed to be the mildest of these sugar alcohols in causing gastrointestinal problems.

So I can't chew trident, etc.

Yea, anything that does screw with my stomach seems to cause the nervous spasm.

And I found that in my case, like Frangible, that meditation and such were very helpful, but they still didn't stop the spasm and within a few minutes I would be nervous again.

Nothing did, unless I worked on helping the stomach out first, physiologically.

I've been re-reading "Confessions of an English Opium-eater" and he (obviously really brilliant guy, ahead of his time) describes a strange "stomach spasm" that arose after an extended period of starvation in his youth. Very interesting. A lot of people seem to allude to odd stomach problems.

*except when it flared up a few weeks ago, which lead to me to stay awake for more than 72 hours straight at several points. The shitty thing is that it gets much, much worse under emotional stress or sleep deprivation -- and if it's happening, being utterly exhausted beyond belief simply does not work to let me sleep. During this period I fucked up my life a bit and pretty much destroyed my relationship with my (ex)girlfriend. Shitty.
Sanction
QUOTE (Frangible @ Apr 16 2008, 11:53 AM) *
from my body's standpoint nearly choking to death several times is a pretty traumatic basic survival issue. I always assumed though that such a reaction would make me feel significant psychological anxiety, arousal, and distress, but it did not. Maybe my assumptions were just wrong.
The evidence for one-trial learning from food poisoning makes me pretty certain that your gut can act like a sentient learner without any awareness in the CNS. In evolutionary terms, the gut's intelligence formed million of years before the lump in the cranium grew up. So yeah, threats to survival can be encoded in the gut without sending a memo to the head.

An analogy: Suppose my ex-girlfriend is the Gut and I'm the Brain. As the Gut, she thinks...um... whatever the fuck she thinks, and doesn't explain it to me in clear English. Probably she can't explain it. Too busy squeezing every nutrient out of what I give her and storing up toxins. I mean, every day she turns enjoyable meals into shit and doesn't give a damn what I think or feel about her actions.

Hey not a bad analogy. Furthermore I still have the brain and she still has the gut.
Oh, man, that comment was rude. Even nasty. Sorry.
(Note to Self: still have anger around ex-GF; deal with it.)

In a previous ancient thread I described how I used the onset of influenza and nausea to quit smoking. I had learned about the power of sickness to quickly condition animal behavior. So, whenever I felt a wave of nausea I would imagine cigarettes, the smell of smoke, etc. Paired-association.

By the time the flu was gone the thought of smoking was literally nauseating. I didn't pick up a cigarette again for 12 years. DIY Clockwork Orange.

Side note: I read about one engineer who spend two years trying to find which food gave his wife IBS-type reactions. Meticulously they did elimination diets on all her foods. Finally, he narrowed it down to salt. SALT? I have no explanation (and neither did he) as to why symptoms were reliably related to the amount of salt in her food. Why do I mention this? It's just so frickin' weird that it must mean something.
ozzman
So all our gut problems are mostly in our heads? Pavlovian responses and all.

[anecdote]I have been able to stop my explosive IBS symptoms at times (when I hadn't been taking probiotics for a while) merely by willing them away. Deep breathing, relaxation and finally relief. Can only be done with a bathroom nearby, for safety, kinda like having a spotter.[/anecdote]
Frangible
It's certainly tricky/interesting. It can be in our head, certainly. But the enteric nervous system is pretty huge mass of reptilian intelligence unto itself-- it has more neurons than the spinal cord.

QUOTE
http://www.scholarpedia.org/article/Enteric_nervous_system

Control of Motility

The progress of the contents in an oral to anal direction is inhibited when sympathetic nerve activity increases. To achieve this, transmission from enteric excitatory reflexes to the muscle is inhibited and the sphincters are contracted. The post-ganglionic sympathetic neurons utilise noradrenaline as the primary transmitter. Under resting conditions, the sympathetic pathways exert little influence on motility. They come into action when protective reflexes are activated.


So wait. Anxiety should elevate NE and decrease bloating/diarrhea, not increase it. This makes sense, since you don't really need to feel an overwhelming desire to take a crap when a bear/velociraptor/zombie is chasing you.

QUOTE
Defense reactions

Enteric neurons are involved in a number of defense reactions of the gut. Defense reactions include diarrhea to dilute and eliminate toxins, exaggerated colonic propulsive activity that occurs when there are pathogens in the gut, and vomiting.

Fluid secretion is provoked by noxious stimuli, particularly by the intraluminal presence of certain viruses, bacteria and bacterial toxins. This secretion is due in large part to the stimulation of enteric secretomotor reflexes. The physiological purpose is undoubtedly to rid the body of pathogens and their products. However, if the pathogens overwhelm the body’s ability to cope, the loss of fluid (diarrhoea) can become a serious threat to the organism.


Ok, so how the fuck does that happen?

QUOTE
Regulation of fluid exchange and local blood flow

The enteric nervous system regulates the movement of water and electrolytes between the gut lumen and tissue fluid compartments. It does this by directing the activity of secretomotor neurons that innervate the mucosa in the small and large intestines and control its permeability to ions. Neurotransmitters of secretomotor neurons are vasoactive intestinal peptide (VIP) and acetylcholine. Secretion is integrated with vasodilatation, which provides some of the fluid that is secreted. Most secretomotor neurons have cell bodies in submucosal ganglia.

Fluxes of fluid, greater than the total blood volume of the body, cross the epithelial surfaces of the gastrointestinal tract each day. Control of this fluid movement via the enteric nervous system is of prime importance for the maintenance of whole-body fluid and electrolyte balance. The largest fluxes are across the epithelium of the small intestine, with significant fluid movement also occurring in the large intestine, stomach, pancreas and gall-bladder. Water moves between the lumens of digestive organs and body fluid compartments in response to transfer of osmotically active molecules. The greatest absorption of water, 8-9 litres per day, accompanies inward flux of nutrient molecules and Na+ through the activation of nutrient co-transporters, and the greatest secretion accompanies outward fluxes of Cl¯ and HCO3¯ in the small and large intestine, gall-bladder and pancreas. In each of these organs, fluid secretion is controlled by enteric reflexes. In the small intestine and most of the colon the reflexes circuits are intrinsic, in the enteric nervous system. They balance secretion with absorptive fluxes, and draw water from the absorbed fluid and from the circulation. The activity of the secretomotor reflexes is under a physiologically important control from inhibitory sympathetic nerve pathways that respond to changes in blood pressure and blood volume through central reflex centres.


So this seems to mostly be related to VIP (wtfever that is) and ACh and the role of the CNS is inhibitory. It seems to me the CNS can cause constipation, but not diarrhea.

Going back to my azn food thing-- maybe there was something about the water I drank before the meal came that set my ENS off. Some like, trace chemical leftover from laundry detergent or some shit.

QUOTE
ENS-CNS interactions

The gastrointestinal tract is in two way communication with the CNS. Afferent neurons convey information about the state of the gastrointestinal tract. Some of this reaches consciousness, including pain and discomfort from the gut and the conscious feelings of hunger and satiety, which are integrated perceptions derived from the gastrointestinal tract and other signals (blood glucose, for example). Other afferent signals, concerning, for example, the nutrient load in the small intestine, or the acidity of the stomach, do not normally reach consciousness. In turn, the CNS provides signals to control the intestine, which are, in most cases, relayed through the ENS. For example, the sight and smell of food elicits preparatory events in the gastro-intestinal tract, including salivation and gastric acid secretion. This is termed the cephalic phase of digestion. Swallowed food stimulates the pharynx and upper esophagus, eliciting afferent signals that are integrated in the brainstem, and subsequently provide efferent signals to enteric neurons in the stomach that cause acid secretion and increased gastric volume, in preparation for the arrival of the food. At the other end of the gut, signals from the colon and rectum are relayed to defecation centres in the spinal cord, from which a programmed set of signals is conveyed to the colon, rectum and anal sphincter to cause defecation. The defecation centres are under inhibitory control from higher CNS regions, and inhibition that can be released when it is chosen to defecate. The other central influences are through sympathetic pathways, which have been discussed under the sections on control of motility and regulation of fluid exchange and local blood flow, above.


I am NOT seeing how the CNS can cause diarrhea from this information.

QUOTE
Neuro-immune interactions

Two-way communication occurs between the enteric nervous system and the immune system of the gastrointestinal tract, that is, transmitters released by the terminals of enteric neurons in the mucosa influence immune-related cells, such as mast cells, and the cells of the mucosa release active substances, including cytokines and mast cell tryptase, that act on enteric neurons (De Giorgio et al. 2004; Lomax et al. 2006). The inter-communication that occurs in disorders such as Crohn’s disease and ulcerative colitis are complex, and beyond the scope of this short review.


So I'm sure part of the sensation of toxins/pathogens as mentioned above is carried out by the immune system. Unfortunately, meditation doesn't make you sneeze any less if you have a pollen allergy, so I'm not sure the CNS can do much here either than direct the body to take drugs or get immune therapy. Or avoid the offending trigger.
ozzman
QUOTE (Frangible @ Apr 18 2008, 02:49 PM) *
It's certainly tricky/interesting. It can be in our head, certainly. But the enteric nervous system is pretty huge mass of reptilian intelligence unto itself-- it has more neurons than the spinal cord.



So wait. Anxiety should elevate NE and decrease bloating/diarrhea, not increase it. This makes sense, since you don't really need to feel an overwhelming desire to take a crap when a bear/velociraptor/zombie is chasing you.


Haven't you heard that when (if) a bear/velociraptor/zombie is chasing you, some may shit themselves ... for real, I shit you not.


You brought the allergies thing, compromised immune systems are prone to asthma, food allergies, eczema, IBS all because we don't let kids eat a little dirt now and then. You see, in the developed world we are too clean, our gut flora is worked overtime and in some cases it is severely lacking.

*************************

Paediatr Perinat Epidemiol. 2007 Nov;21 Suppl 3:23-8. Links
Examining the hygiene hypothesis: the Trial of Infant Probiotic Supplementation.
Cabana MD, McKean M, Wong AR, Chao C, Caughey AB. Department of Pediatrics, University of California, San Francisco, CA 94118, USA. michael.cabana@ucsf.edu

The hygiene hypothesis suggests that the absence of infectious exposure at a critical point in immune system development leads to a greater risk for the later development of atopic disease. As a result, it may be possible to devise strategies that can block the onset of atopic diseases such as asthma. This paper outlines the rationale, background and design for the Trial of Infant Probiotic Supplementation study, which is designed to test the effectiveness of a daily infant probiotic supplement in the first 6 months of life in preventing the development of early markers of asthma.

PMID: 17935572

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Adv Exp Med Biol. 2008;606:423-54.Links
Probiotics, immunomodulation, and health benefits.
Gill H, Prasad J. Department of Primary Industries, Werribee, Victoria 3030, Australia. Harsharn.Gill@dpi.vic.gov.au

Probiotics are defined as live microorganisms that, when administered in adequate amount, confer a health benefit on the host. Amongst the many benefits associated with the consumption of probiotics, modulation of the immune system has received the most attention. Several animal and human studies have provided unequivocal evidence that specific strains of probiotics are able to stimulate as well as regulate several aspects of natural and acquired immune responses. There is also evidence that intake of probiotics is effective in the prevention and/or management of acute gastroenteritis and rotavirus diarrhoea, antibiotic-associated diarrhoea and intestinal inflammatory disorders such as Crohn's disease and pouchitis, and paediatric atopic disorders. The efficacy of probiotics against bacterial infections and immunological disorders such as adult asthma, cancers, diabetes, and arthritis in humans remains to be proven. Also, major gaps exist in our knowledge about the mechanisms by which probiotics modulate immune function. Optimum dose, frequency and duration of treatment required for different conditions in different population groups also remains to be determined. Different probiotic strains vary in their ability to modulate the immune system and therefore efficacy of each strain needs to be carefully demonstrated through rigorously designed (randomised, double-blind, placebo-controlled) studies. This chapter provides an over view of the immunomodulatory effects of probiotics in health and disease, and discusses possible mechanisms through which probiotics mediate their disparate effects.

PMID: 18183940

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Allergy. 2007 Nov;62(11):1223-36. Epub 2007 Aug 17. Links
The role of the intestinal microbiota in the development of atopic disorders.
Penders J, Stobberingh EE, van den Brandt PA, Thijs C. Department of Epidemiology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands.

The prevalence of atopic diseases, including eczema, allergic rhinoconjunctivitis and asthma, has increased worldwide, predominantly in westernized countries. Recent epidemiological studies and experimental research suggest that microbial stimulation of the immune system influences the development of tolerance to innocuous allergens. The gastrointestinal microbiota composition may be of particular interest, as it provides an early and major source of immune stimulation and seems to be a prerequisite for the development of oral tolerance. In this review the observational studies of the association between the gut microbiota and atopic diseases are discussed. Although most studies indicated an association between the gut microbiota composition and atopic sensitization or symptoms, no specific harmful or protective microbes can be identified yet. Some important methodological issues that have to be considered are the microbiological methods used (traditional culture vs molecular techniques), the timing of examining the gut microbiota, the definition of atopic outcomes, confounding and reverse causation. In conclusion, the microbiota hypothesis in atopic diseases is promising and deserves further attention. To gain more insight into the role of the gut microbiota in the etiology of atopy, large-scale prospective birth cohort studies using molecular methods to study the gut microbiota are needed.

PMID: 17711557

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Pharmacotherapy. 2008 Apr;28(4):496-505. Links
Effectiveness of probiotics in the treatment of irritable bowel syndrome.
Wilhelm SM, Brubaker CM, Varcak EA, Kale-Pradhan PB. 1 Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Harper University Hospital, Detroit, Michigan.

Abstract Recently, the use of tegaserod and alosetron-drugs approved for the treatment of irritable bowel syndrome (IBS)-has been restricted because of adverse events. This has resulted in a need for additional modalities for the treatment of IBS. Our objective was to determine the effectiveness of probiotics in the global relief of symptoms associated with IBS and in the improvement of flatulence, abdominal pain, transit time, and bacterial counts. Using the MEDLINE database from 1966-October 2007 and manually searching article references for relevant articles and abstracts, we identified 14 blinded, placebo-controlled clinical trials of the effectiveness of probiotics in the treatment of IBS. Of 11 studies in which overall symptom relief was assessed, seven indicated a significant improvement with probiotics versus placebo. Five of eight investigations of abdominal pain and distention revealed a benefit with probiotic use. Four studies demonstrated an improvement in symptomatic flatulence in probiotic treatment groups, whereas one study showed no significant benefit. Four of five studies of the effects of probiotics on colonic transit time revealed a benefit compared with placebo. As probiotics have shown benefit and possess a favorable adverse-effect profile, their use may represent an option for symptom relief in patients with IBS. However, additional data are necessary before probiotics can become a standard of care in the treatment of IBS, a complex and chronic condition.

PMID: 18363533

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Behav Res Ther. 2001 Jul;39(7):801-11. Links
The effects of relaxation response meditation on the symptoms of irritable bowel syndrome: results of a controlled treatment study.
Keefer L, Blanchard EB. The University at Albany, State University of New York, Center for Stress and Anxiety Disorders, 12203, USA.

In this study, Herbert Benson's (1975) Relaxation Response Meditation program was tested as a possible treatment for Irritable Bowel Syndrome (IBS). Participants were 16 adults who were matched into pairs based on presence of Axis I disorder, primary IBS symptoms and demographic features and randomized to either a six week meditation condition or a six week wait list symptom monitoring condition. Thirteen participants completed treatment and follow-up. All subjects assigned to the Wait List were subsequently treated. Patients in the treatment condition were taught the meditation technique and asked to practice it twice a day for 15 minutes. Composite Primary IBS Symptom Reduction (CPSR) scores were calculated for each patient from end of baseline to two weeks post-treatment (or to post wait list). One tailed independent sample t-tests revealed that Meditation was superior to the control (P=0.04). Significant within-subject improvements were noted for flatulence (P=0.03) and belching (P=0.02) by post-treatment. By three month follow-up, significant improvements in flatulence (P<0.01), belching (P=0.02), bloating (P=0.05), and diarrhea (P=0.03) were shown by symptom diary. Constipation approached significance (P=0.07). Benson's Relaxation Response Meditation appears to be a viable treatment for IBS.

PMID: 11419611

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In other words...Buddha didn't get IBS
avantgarde
While this is obviously a promotion of a product I thought the text pretty much sums up the effects of caffeine in IBS :

http://www.teeccino.com/colon.aspx

Brings up a few ideas with can be applied to concepts in this thread I find the GABA-IBS connection interesting (obviously relevant for the stress/anxiety bit).

Ozzman why shouldn´t probiotics be taken chronically ?


ozzman
I don't take them chronically because I'm cheap..So I eat a bunch of critters...then feed them for a while
Frangible
QUOTE (Sanction @ Apr 18 2008, 12:01 PM) *
Side note: I read about one engineer who spend two years trying to find which food gave his wife IBS-type reactions. Meticulously they did elimination diets on all her foods. Finally, he narrowed it down to salt. SALT? I have no explanation (and neither did he) as to why symptoms were reliably related to the amount of salt in her food. Why do I mention this? It's just so frickin' weird that it must mean something.


Sodium ions can play an excitatory role in activating the "KILL IT WITH WATER" response I'd think. Also salt's effects elsewhere in the body may lead to greater sympathetic activation and therefore possible constipation.

QUOTE
In other words...Buddha didn't get IBS


The only thing you could do with your mind here is activate the sympathetic inhibitory pathways (for diarrhea) or release them if they're been held active for too long (for constipation). Kinda ironic if meditation ends up activating the sympathetic nervous system and releasing NE, eh?

Probiotics can obviously affect gas generation, the immune response (via pathogen balance / inflammation), and the rate of digestion via what they metabolize stuff to.
avantgarde
1: J Clin Psychiatry. 1991 Dec;52(12):502-8.Links
An open label trial of alprazolam in comorbid irritable bowel syndrome and generalized anxiety disorder.Tollefson GD, Luxenberg M, Valentine R, Dunsmore G, Tollefson SL.
Department of Psychiatry, St. Paul-Ramsey Medical Center, Minn 55101.

BACKGROUND: The irritable bowel syndrome (IBS) is very prevalent and psychiatric comorbidity runs high. A significant proportion of generalized anxiety disorder (GAD) patients manifest concurrent IBS. METHOD: We conducted a 14-week, open-label trial of the triazolobenzodiazepine alprazolam in 32 patients with comorbid generalized anxiety and IBS. At the end of a 2-week placebo run-in, eligible subjects received 6 weeks of active drug therapy. RESULTS: Ninety-four percent of subjects (N = 25) had a full or partial anxiolytic response at the 6th treatment week (p less than .001). Eighty-nine percent (N = 24) experienced a concomitant reduction in IBS severity. For the majority, these dual benefits were still evident at the conclusion of a 4-week drug taper (p = .05) and achieved a trend (p = .07) at a 4-week postdrug discontinuation visit. CONCLUSION: Alprazolam was safe, effective, and well tolerated during the acute treatment of comorbid GAD and IBS; only a limited posttreatment rebound was observed.
avantgarde
Effect of a second-generation alpha2delta ligand (pregabalin) on visceral sensation in hypersensitive patients with irritable bowel syndrome.Houghton LA, Fell C, Whorwell PJ, Jones I, Sudworth DP, Gale JD.
Neurogastroenterology Unit, Academic Division of Medicine and Surgery, University of Manchester, Wythenshawe Hospital, Southmoor Road, Wythenshawe, Manchester M23 9LT, UK. Lesley.Houghton@manchester.ac.uk

BACKGROUND: Visceral hypersensitivity is an important pathophysiological factor in irritable bowel syndrome (IBS). Pre-clinical studies suggest that the alpha(2)delta ligand pregabalin reduces both visceral allodynia and hyperalgesia, but is inactive on basal sensitivity. AIM: To assess the effect of pregabalin on the perception of rectal distension in hypersensitive IBS patients. METHODS: Twenty-six patients with Rome-II-defined IBS (aged 18-46 years, 7 male) were included in a randomized, double-blind, placebo-controlled, parallel-group study in which they received either 3 weeks oral pregabalin (titrated: 50 mg tid days 1-3, 100 mg tid days 4-7, 150 mg tid days 8-11; fixed 200 mg tid days 12-21 +/-4) or placebo control. Rectal sensitivity was assessed using a barostat technique, in which sensory thresholds were determined using the ascending method of limits, followed by tracking both before and after treatment. Only patients with a pain threshold of <or=28 mmHg were included in the study. RESULTS: Pregabalin significantly increased the sensory thresholds from baseline for first sensation (p = 0.045), desire to defecate (p = 0.008) and pain (p = 0.048) compared with placebo control. In addition, pregabalin significantly increased rectal compliance (p<0.0001), although this appeared to be unrelated to the changes in sensitivity. Despite the occurrence of mild dizziness and somnolence, pregabalin was generally well tolerated. CONCLUSIONS: Pregabalin increased distension sensory thresholds to normal levels in IBS patients with rectal hypersensitivity. A concomitant increase in rectal compliance appeared to be unrelated to the reduction in sensitivity. These data suggest that alpha(2)delta ligands are worthy of further investigation in the treatment of visceral pain disorders, including IBS.
avantgarde
: Aliment Pharmacol Ther. 2005 Nov 15;22(10):981-8. Links
Gabapentin reduces rectal mechanosensitivity and increases rectal compliance in patients with diarrhoea-predominant irritable bowel syndrome.Lee KJ, Kim JH, Cho SW.
Department of Gastroenterology, Ajou University School of Medicine, Suwon, Korea. kjleemd@hotmail.com

BACKGROUND: Gabapentin has been shown to reduce elements of central sensitization in human experimental hyperalgesia. It remains uninvestigated whether gabapentin has beneficial effects for irritable bowel syndrome associated with visceral hypersensitivity. AIMS: To evaluate the effects of gabapentin on sensory and motor function of the rectum in patients with diarrhoea-predominant irritable bowel syndrome. METHODS: Forty patients with diarrhoea-predominant irritable bowel syndrome completed this randomized, double-blind, placebo-controlled, parallel-grouped study. All patients received a barostat study and were subsequently randomized for 5-day treatment with gabapentin 300 mg/day and then 600 mg/day or placebo. On day 6, after subjects had their morning dose, the barostat experiment was repeated. RESULTS: The threshold pressures for bloating, discomfort and pain significantly increased after gabapentin, but not after placebo. Significant increase in the pressure and corresponding wall tension inducing discomfort or pain were observed in the gabapentin group, but not in the placebo group. Rectal compliance significantly increased after gabapentin, but not after placebo. The postprandial increase of rectal tone was not affected by gabapentin. CONCLUSION: Our results show that gabapentin reduces rectal sensory thresholds through attenuating rectal sensitivity to distension and enhancing rectal compliance in diarrhoea-predominant irritable bowel syndrome patients. The clinical efficacy of this drug in irritable bowel syndrome patients warrants investigation.
Frangible
If you're digging up IBS studies make sure they're diarrhea related, most people with IBS seem to be anxious women with constipation. And frankly I don't think that applies to anyone on this forum.

You'll note in diarrhea patients, gabapentin decreased the central perception of pain, but didn't actually change the increase in gastrointestinal tone. All the more evidence central anxiety/pain have little to do with diarrhea.
avantgarde
I belive there are 3 types - C,D, and a "mixed" category.

And "bloating" seems to be present in all 3 categories ?

The studies all were on GABAergic drugs. You , me and everybody posting in this thread describes IBS as getting worse during times of stress.

Stimulants do a number on GABA and again you, me and everybody in this thread use stimulants which lower GABA.

This sounds really stupid but I think somehow constipation and diarrhea might be affected by the same factors discussed in this thread and I don´t think it´s a simple as too little X equals constipation while to much X gives diarrhea. It might be a disrupted balance and if you fiddle with X then Y might be affected also.

Kind of how some people on M2 take deprenyl to threat depression. The extra dopamine is cool for a brief period then the cascade of events leads to lowered serotonin and they feel "burned out", "OCD" and "like shit".






Frangible
QUOTE
You , me and everybody posting in this thread describes IBS as getting worse during times of stress.


Gaaah. Don't fucking say IBS without a qualifier in a discussion like this. When I've had it happen I wasn't stressed at all. The research I showed above indicates stress can contribute to constipation, but again... not relevant to me.

For diarrhea, I see no evidence whatsoever psychosocial stress can do anything but reduce its severity. That's because the only input the CNS has into this process is inhibitory via adrenergic transmission.

Could I be wrong, and you be right? Sure. But I'm gonna need to see SCIENCE before I can accept something that contradicts both my personal experience and research.

QUOTE
The studies all were on GABAergic drugs.


The only effects of GABA were on the central perception of pain. It did NOT effect the colonic tone. The patients had diminished awareness, not diminished diarrhea.

QUOTE
Stimulants do a number on GABA


They actually increase it as a negative feedback response:

http://www.ncbi.nlm.nih.gov/pubmed/1761861...Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/9680244...Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/1182306...Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/1042841...Pubmed_RVDocSum

(though I suspect the increases at typical human doses are marginal to nonexistent)
Proton Soup
QUOTE (Sanction @ Apr 18 2008, 10:01 AM) *
The evidence for one-trial learning from food poisoning makes me pretty certain that your gut can act like a sentient learner without any awareness in the CNS. In evolutionary terms, the gut's intelligence formed million of years before the lump in the cranium grew up. So yeah, threats to survival can be encoded in the gut without sending a memo to the head.


the strongest memories are smells. there's your survival mechanism. i think it's the limbic system in the brain that regulates this.
Frangible
There's the learned taste aversion that you mention (which triggers vomiting), and there is also something wholly in the ENS that triggers diarrhea. So there are at least two different defensive responses.
zuper1
Frangie,do you practise 'belly breathing',either as an single exercise either while you meditate?

I've noticed when I reach the level to completely breath from the abdomen,(expanding on inhalation),with as little effort as possible,a pulsation feeling in the stomach area..

You should benefit with this IMO.
Maybe the 'gut's brain' ...
Frangible
Yes, and I do it outside of meditation as well. I've had spasms in the abdominal area if I have severe enough diarrhea and they've been over-contracted.

I've also started taking probiotics, which hasn't really done anything yet, but I'll give it a little time.
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