Mike's GI Madness - mle_ii journal

[mle_ii]

Mike wow-

Nuts, greens, beef, fruits, all things that would bother me!! Nuts are high in fiiber and might be upsetting your system a little.

Fruits like peach, organges, and bananas cause some people problems especialy the acidic fruits. Maybe try applesauce - unsweetened.

This diet wont work right away. It took me 2 months to see noticable changes.

No probelms with nuts (though some types I might), greens, beef, fiber. So fruits are ok but in small amounts. Most of the posts you read about what I ate were before I found out about fructose being a problem. Though some of those might give me problems during a flareup. Applesauce would send me to the toilet, it's one of the worst for me with the high fructose content.

For the most part my diet is working, just a few things here and there bother me, but there is some thing going on endocrine wise as well that I'm going to have an endocrinologist/interalist look into.

Thanks,
Mike

[thedell19]

That is interesting about no Bifido-

Out of all those tests- which helped you the most to get on target?

[thedell19]

And can you get the USBIO labs tek tests ordered or do you have to get your DR to order them etc.

[mle_ii]

That is interesting about no Bifido-

Out of all those tests- which helped you the most to get on target?

Well that all depends, since I'm still a work in progress it's hard to say. But I'd lean towards the stool testing or at least finding out what bacteria are or are not present and the amounts. Though the enterolab tests were pretty profound, it only really substatiated what I thought. And at least my family doesn't think I'm nutso. LOL Also the allergy testing only really confirmed what I had thought since it didn't really find much new, same with the fructose malaabsorption.

And can you get the USBIO labs tek tests ordered or do you have to get your DR to order them etc.

Good question, I think that Dr had to order them, and if you want to try for insurance coverage then you'd have to do that for sure, but make sure of the coverage before hand if you're looking for that.

Mike

[mle_ii]

This a report from my Nat Dr back in July 2005. Just puting it here for my records. Nothing to see here. :)

Here’s a summary of your labs:
Low Chloride: stomach (acid/hydrochloric acid), adrenals need support
High Protein: Liver, adrenals need support
High Albumin: Liver
High Albumin/Globulin: Liver
Low Alkaline Phosphatase: Low Zinc

[mle_ii]

Stuff on mercury, you can ignore if you want. :)

Mercury depletes glutathione.

Selenium can help remove/detoxify mercury. Not sure, but it appears so.

The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum

Selenium and antioxidant defenses as major mediators in the development of chronic heart failure.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum

Increased oxidative stress is involved in the pathogenesis of chronic heart failure (CHF), the common end result of most cardiac diseases. Selenium is an "essential" trace element, which means that it must be supplied by our daily diet and that its blood and tissue concentrations are extremely low. Selenium has a variety of functions. It is a key component of several functional selenoproteins required for normal health. The best known of these are the antioxidant glutathione peroxidase (GPx) enzymes, which remove hydrogen peroxide and the harmful lipid hydroperoxides generated in vivo by oxygen-derived species. GPx deficiency exacerbates endothelial dysfunction, a major contributing factor in the severity of CHF symptoms, in various conditions such as hyperhomocysteinemia. This suggests that homocysteine may be involved in the CHF associated endothelial dysfunction through a peroxide-dependent oxidative mechanism. Selenium also plays a role in the control of thyroid hormone metabolism and in protection against organic and inorganic mercury. One possible additional mechanism by which low selenium may compromise cardiovascular condition may be through the effect of selenium on the synthesis and activity of deiodinases, enzymes converting thyroxin into the biologically active triiodothyronine. Selenium and iodine actually interact in cardiovascular physiology, and further studies are needed to examine their role, in isolation and in association, in the development of CHF. Thus, selenium (through its role in selenoenzymes, thyroid hormones, and interactions with homocysteine and endothelial function) appears to be a major mediator in several pathways potentially contributing to CHF development.

Whole blood mercury and selenium concentrations in a selected Austrian population: does gender matter?
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum

The roles of serum selenium and selenoproteins on mercury toxicity in environmental and occupational exposure.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum

Many studies have found that mercury (Hg) exposure is associated with selenium (Se) accumulation in vivo. However, human studies are limited. To study the interaction between Se and Hg, we investigated the total Se and Hg concentrations in body fluids and serum Se-containing proteins in individuals exposed to high concentrations of Hg. Our objective was to elucidate the possible roles of serum Se and selenoproteins in transporting and binding Hg in human populations. We collected data from 72 subjects: 35 had very low Hg exposure as evidenced by mean Hg concentrations of 0.91 and 1.25 ng/mL measured in serum and urine, respectively; 37 had high exposure (mean Hg concentrations of 38.5 and 86.8 ng/mL measured in serum and urine, respectively). An association between Se and Hg was found in urine (r = 0.625; p < 0.001) but not in serum. Hg exposure may affect Se concentrations and selenoprotein distribution in human serum. Expression of both selenoprotein P and glutathione peroxidase (GSH-Px) was greatly increased in Hg miners. These increases were accompanied by elevated Se concentrations in serum. In addition, selenoprotein P bound more Hg at higher Hg exposure concentrations. Biochemical observations revealed that both GSH-Px activity and malondialdehyde concentrations increased in serum of the Hg-exposed group. This study aids in the understanding of the interaction between Se and Hg. Selenoproteins play two important roles in protecting against Hg toxicity. First, they may bind more Hg through their highly reactive selenol group, and second, their antioxidative properties help eliminate the reactive oxygen species induced by Hg in vivo.

Co-consumption of selenium and vitamin E altered the reproductive and developmental toxicity of methylmercury in rats.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum

Methylmercury (MeHg), an environmental contaminant primarily found in fish and seafood, may pose long-term health risks to pregnant women and their developing children. The objective of this study was to determine whether co-consumption of nutritional supplements would alter the effects of MeHg on reproductive and developmental toxicity using a rodent model. Adult female rats were fed a diet containing additional selenium (1 ppm), additional vitamin E (225 IU/kg) or a combination of the two for 4 weeks before oral dosing of MeHg (1.25 mg/kg/day). Treatment with MeHg and dietary supplementation continued throughout pregnancy after which the dams were allowed to deliver their offspring. In addition to routine evaluations including periodic body weight measurements and daily clinical signs observations, dams and pups were evaluated for auditory startle habituation and pups were evaluated for developmental landmarks and reflexology. The dams and offspring were euthanized approximately 4 weeks after birth of the offspring. Results indicated that treatment with MeHg caused adverse effects on both reproduction of the dams and decreased progeny survival. However, the dams showed significant improvement in body weight gain during lactation and average auditory startle response time when the diet was enriched with both selenium and vitamin E. The combination of both vitamin E and Se also resulted in a significant increase in post-natal survival when compared to MeHg-treated group. There was no nutrient effect on the MeHg toxicity shown in offspring physical landmarks, performance in reflex tests and assessment of simple auricular startle response. Also, accelerated development as indicated by earlier opening in the pups of the supplemental diet groups was observed. These results suggest that antioxidant nutrients in the diet may alter MeHg reproductive and developmental toxicity. The underlying and human health implications warrant further investigations.

[mle_ii]

More things you can ignore if you wish just trying to keep track of something else.

SIBO and/or methane producing bacteria are known to reduce serotonin.

Low serotonin is associated with several things: (3)
Low body Temp - Thermoregulation (1,2).
Anxiety/Panic Attacks
Gut motility (too much you get diarrhea, too little constipation?)
IBS
Depression
Obsessive Compulsive behaviors
Bipolar
Circadian rythems (sp)
tinnitus
Migraine
Low Blood Pressure

Whoa, I wonder about liver disease, thus detox. It appears that serotonin plays a part in liver regeneration. (4) Given that the liver is involved in glutathione might liver damage not being rebuilt by having low serotonin levels cause depleted levels of glutathione?


1) Serotonin and thermoregulation: old and new views.
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

An overview is presented of the evidence favouring a pivotal role for serotoninergic neurons in the diencephalon's control system for body temperature. 1. Morphological investigations of the anterior hypothalamus reveal that 5-HT injected locally into this thermosensitive zone evokes a hyperthermia in virtually all species. Pharmacological blocking agents of serotoninergic receptors antagonize the 5-HT-induced rise in an animal's temperature. 2. Further, the destruction of serotoninergic neurons in the anterior hypothalamic pre-optic area of a rat or monkey severely impairs the heat production responses during cold stress. 3. In addition, the release of 5-HT from anterior hypothalamic tissue is enhanced significantly when the animal is exposed to a cold environmental temperature, and subsequently shivers, vasoconstricts and conserves heat. 4. New observations are described which show that 5-HT may elicit a fall in temperature as a result of the: (1) overloading of 5-HT receptor sites in the anterior hypothalamus; and/or (2) occupation by 5-HT of either noradrenergic or dopaminergic receptors, or both classes of catecholamine receptors which are believed to mediate the hypothalamic pathways for heat loss. 5. Finally, new data also implicate neuronal 5-HT, again only within the anterior hypothalamic pre-optic area, in the cellular mechanism which triggers a fever in response to a bacterial challenge. Thus, the serotoninergic neurons underlying the rostral hypothalamic temperature controller are responsible not only for the defense of an animal's body temperature during exposure to cold, but also for initiating the shift in the temperature "set-point" during a febrile episode.

2) http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
Depletion of the lipid raft constituents, sphingomyelin and ganglioside, decreases serotonin binding at human 5-HT(7(a)) receptors in HeLa cells.

5-HT(7) receptors are involved in the regulation of depression, circadian rhythms, thermoregulation and vasodilatation.

3) http://en.wikipedia.org/wiki/Serotonin

In the central nervous system, serotonin is believed to play an important role in the regulation of anger, aggression, body temperature, mood, sleep, vomiting, sexuality, and appetite. Low levels of serotonin have been associated with several disorders, namely increase in aggressive and angry behaviors, clinical depression, Obsessive-compulsive disorder (OCD), migraine, irritable bowel syndrome, tinnitus, fibromyalgia, bipolar disorder, anxiety disorders[citation needed] and intense religious experiences[1].

4) Platelet-derived serotonin mediates liver regeneration.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=16601191

The liver can regenerate its volume after major tissue loss. In a mouse model of liver regeneration, thrombocytopenia, or impaired platelet activity resulted in the failure to initiate cellular proliferation in the liver. Platelets are major carriers of serotonin in the blood. In thrombocytopenic mice, a serotonin agonist reconstituted liver proliferation. The expression of 5-HT2A and 2B subtype serotonin receptors in the liver increased after hepatectomy. Antagonists of 5-HT2A and 2B receptors inhibited liver regeneration. Liver regeneration was also blunted in mice lacking tryptophan hydroxylase 1, which is the rate-limiting enzyme for the synthesis of peripheral serotonin. This failure of regeneration was rescued by reloading serotonin-free platelets with a serotonin precursor molecule. These results suggest that platelet-derived serotonin is involved in the initiation of liver regeneration.

[mle_ii]

More on SIBO. It appears that my fructose/lactose intollerance may not even be the case. In a nutshell if I have SIBO then those foods containing fructose/lactose would show symptoms of malabsorption. Thus leading to a false positive. The more likely case would be that once I treat and am cured of SIBO that I will no longer have symptoms of malabsorption of fructose and/or lactose.

Breath Testing to Evaluate Lactose Intolerance in Irritable Bowel Syndrome Correlates With Lactulose Testing and May Not Reflect True Lactose Malabsorption
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum

OBJECTIVES: An increased prevalence of lactose intolerance is seen in irritable bowel syndrome (IBS). Recently, we demonstrated a high prevalence of abnormal lactulose breath test results in IBS suggesting bacterial overgrowth. Because symptoms of lactose intolerance result from bacterial fermentation, the purpose of this study was to determine whether an abnormal lactose breath test is reflective of malabsorption or early presentation to bacteria. METHODS: Subjects with diarrhea-predominant IBS were enrolled. On day 1, subjects underwent a lactulose breath test after an overnight fast. Within 1 wk, subjects returned after fasting for a lactose breath test with simultaneous blood glucose measurements every 15 min to complete a lactose tolerance test (LTT). Symptoms were evaluated 3 h after lactose administration. RESULTS: Twenty subjects completed the study. One subject inadvertently received dextrose through the intravenous and was excluded. Of the remaining 19 subjects, three (16%) had an abnormal LTT suggesting malabsorption. In all, 10 subjects (53%) had an abnormal lactose breath test, 14 (74%) had an abnormal lactulose breath test, and 11 (58%) had symptoms after lactose administration. The agreement with symptoms was moderate (kappa = 0.47) and fair (kappa = 0.24) when compared to the lactose breath test and LTT, respectively. There was a fair correlation between lactose breath test and LTT (kappa = 0.29). However, lactose breath test hydrogen levels >166 ppm were universally predictive of abnormal LTT. Finally, a significant correlation was seen between the hydrogen production on lactose and lactulose breath test (r = 0.56, p = 0.01). CONCLUSIONS: Lactose breath testing in IBS subjects does not seem to reflect malabsorption; it may be an indicator of abnormal lactulose breath test, suggesting bacterial overgrowth.

[mle_ii]

Please ignore just looking for studies on Methane and effects on the body.

The degree of breath methane production in IBS correlates with the severity of constipation.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=17397408

Am J Gastroenterol. 2007 Apr;102(4):837-41.
BACKGROUND: Recent work has demonstrated that among irritable bowel syndrome (IBS) subjects, methane on lactulose breath test (LBT) is nearly universally associated with constipation predominance. This work has been based on subjective constipation outcomes. In this study, methane is compared to constipation in another population of IBS subjects with constipation being determined both subjectively and objectively. METHODS: A nested study was conducted in subjects enrolled in a double-blind randomized placebo-controlled study. After consent, subjects were asked to complete a stool diary for 7 days. This included logging of all bowel movements that week as well as documenting the stool consistency for each during the same period using the Bristol Stool Score. After 7 days, subjects were asked to rate their symptoms on a visual analogue scale (VAS) score (0-100 mm) for diarrhea and constipation. They then had an LBT to evaluate both methane and hydrogen profiles over 180 min. Subjects with methane were compared to those without methane for Bristol Stool Score, stool frequency, as well as VAS scores for diarrhea and constipation. The degree of constipation was then compared to the quantity of methane production on LBT based on area under the curve. RESULTS: Among 87 subjects, 20 (23.8%) produced methane. IBS subjects with methane had a mean constipation severity of 66.1 +/- 36.7 compared to 36.2 +/- 30.8 for nonmethane producers (P < 0.001). The opposite was noted for diarrhea (P < 0.01). On LBT, the quantity of methane seen on breath test was directly proportional to the degree of constipation reported (r = 0.60, P < 0.01). In addition, greater methane production correlated with a lower stool frequency (r =-0.70, P < 0.001) and Bristol Stool Score (r =-0.58, P < 0.01). CONCLUSION: Methane on LBT is associated with constipation both subjectively and objectively. The degree of methane production on breath test appears related to the degree of constipation.

Effect of resistant starch on breath-hydrogen and methane excretion in healthy volunteers.
http://www.ncbi.nlm.nih.gov/sites/entre ... ds=8116539
http://www.ajcn.org/cgi/reprint/59/3/626

Am J Clin Nutr. 1994 Mar;59(3):626-30.
Colonic fermentation of dietary carbohydrates and fiber might produce a protective effect against the development of large bowel cancer. Resistant starch, ie, starch that escapes small bowel digestion, is a candidate fermentable substrate that has been hitherto little studied. We supplemented 19 healthy volunteers with 15 g native amylomaize (Hylon-VII) three times a day, containing 28 g type II resistant starch, or with dextrins as a placebo for 7 d in a crossover design. Pre-experimentally, 11 subjects regularly produced breath methane and 8 did not. Resistant starch increased 24-h integrated excretion of breath hydrogen. The mean rise relative to placebo was 35% (P = 0.03) for all subjects and 60% for eight subjects not producing methane (P = 0.02). The 11 methane producers showed a 93% increase in breath-methane excretion on resistant starch (P = 0.03). Continued consumption of 28 g type II resistant starch/d is well tolerated and increases colonic fermentation in healthy volunteers.

Breath hydrogen response to lactulose in healthy subjects: relationship to methane producing status.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=2323593

Gut. 1990 Mar;31(3):300-4
In order to assess the relationship between methane (CH4) producing status and the breath excretion of hydrogen (H2) in healthy subjects, breath CH4 and H2 were simultaneously measured for 14 hours after oral ingestion of 10 g lactulose in 65 young volunteers. Forty were breath CH4 producers and 25 were not. Statistically significant differences were observed between both groups, with lower values for CH4 producers recorded for the following parameters: fasting basal value of breath H2 (8.1 (4.9) v 5.2 (3.7) ppm, p less than 0.05), mouth-to-caecum transit time (68 (24) v 111 (52) min, p less than 0.005), and breath H2 production measured as area under the curve 13.1 (6.9) v 8.8 (3.8) 10(3) ppm/min, p less than 0.02). There was no significant correlation between individual production of breath H2 and CH4. These results indicate that the response to lactulose depends on breath CH4 producing status. In clinical practice, defining normal values of mouth-to-caecum transit time without knowledge of breath CH4 producing status may lead to misinterpretation of the H2 breath test.

Pulmonary hydrogen and methane excretion following ingestion of an unabsorbable carbohydrate: a study of twins.
http://www.ncbi.nlm.nih.gov/sites/entre ... stractPlus

J Pediatr Gastroenterol Nutr. 1985 Dec;4(6):936-41.
Pulmonary excretion of hydrogen and methane after administration of an unabsorbable disaccharide (lactulose) was determined in 228 adult Hungarian twins, 60 monozygous (MZ) and 54 dizygous (DZ) pairs. More than 98% of the subjects (224 of 228) excreted large amounts of hydrogen between 90 and 180 min after lactulose administration. Methane excretion in the fasting state was observed in 124 of 228 of the probands (54.4%), and 68 of 228 (29.8%) produced additional methane in response to lactulose ingestion. In contrast to hydrogen production, both methane excretion and production were significantly more frequent in females than in males. In the total group, and more distinctly in females, the correlation between peak hydrogen and methane concentrations was negative. Twin concordance of fasting methane excretion and lactulose-induced methane production was near 70% in both MZ and DZ pairs. Heritability estimates of methane excretion and production based on intrapair correlation and variance were smaller than unity, and intrapair correlation coefficients were larger in twin pairs living apart than in those living in the same household. Methane excretion is comparatively frequent in the Hungarian population, and a substantial proportion of fasting methane excreters (55%) produce additional methane from lactulose. The sex difference of methane excretion appears to be characteristic of European populations. The twin data disprove regular Mendelian inheritance of methane production and are suggestive of genetic effects in a multifactorial system.

Relationships between hydrogen (H2) and methane (CH4) production in man.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=7167741

Scand J Gastroenterol. 1982 Nov;17(8):985-92
The H2 breath test was performed by ingestion of 33 g lactulose and analysis of end-expiratory air. Eight of 100 healthy subjects failed to produce significant amounts of H2. The test was repeated twice in these eight subjects. Four had a flat excretion curve in all three tests, and all excreted large amounts of breath CH4. Of the 100, 34 had breath CH4 above 0.5 mumol/l. They had significantly lower fasting breath H2 and breath H2 excretion after lactulose than the 66 with breath CH4 below 0.5 mumol/l (p less than 0.01). By means of a gas chromatographic method with high sensitivity for CH4, 33 of the 100 subjects were restudied with parallel measurement of pulmonary excretion of H2 and CH4. Typical patterns of excretion were found in the subjects with endogenous CH4 production, showing either high excretion of H2 and low CH4 or low H2 and high CH4. A combination of high H2 and high CH4 was never seen. These findings suggest that CH4 is produced in the human intestine chiefly by an H2-utilizing flora and that adequate assessment of gut bacterial carbohydrate fermentation would require parallel measurement of breath H2 and CH4. The prevalence of CH4 production in a group of 120 healthy subjects, determined by a single midday breath sample, was 44%, with no significant difference between sexes and no correlation to age. Repeated midday breath sampling in 12 subjects during 1 month proved this method to be very reliable in the assessment of an individual's ability to produce CH4.

Intestinal hydrogen and methane of men fed space diet.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=12197533

Life Sci Space Res. 1969;7:102-9
Intestinal bacteria form two gases, hydrogen (H2) and methane (CH4), that could constitute a fire hazard in a closed chamber. So H2 and CH4 pass from the anus but these gases are also transported by the blood to the lungs and removed to the atmosphere. Several factors affect gas formation: 1) amount and kind of fermentable substrate; 2) abundance, types, and location of microflora; and 3) psychic and somatic conditions that affect the gut. We evaluated the first factor by studying men fed different diets and have also recorded influences of uncontrollable factors. One group of 6 men ate Gemini-type diet (S) and another received a bland formula (F), for 42 days. Breath and rectal gases were analyzed during the first and final weeks. Flatus gases varied widely within dietary groups but much more gas was generated with diet S than with F. In the first 12-hour collection, subjects fed S passed 3 to 209 ml (ATAP) of rectal H2 (avg 52) and 24 to 156 ml (avg 69) from the lungs (assuming normal pulmonary ventilation). With F, these values were 0 to 3 ml (avg 1) and 6 to 36 ml (avg 20). Subjects were calmer during the second test. Gas production was lower with S than initially; F values were unchanged. Methane differed idiosyncratically, presumably due to differences in flora. Computed from 12-hour values, maximum potential daily H2 and CH4 are per man: for S, 730 ml and 382 ml; for F, 80 and 222 ml. Volumes would be larger at reduced spacecraft and suit pressures.

http://www.ncbi.nlm.nih.gov/sites/entre ... ch=6283045
http://jn.nutrition.org/cgi/reprint/112/6/1133
Excretion of breath and flatus gases by humans consuming high-fiber diets.

The abilities of dietary fibers to promote the excretion of intestinal fermentation gases were evaluated in five healty men. Flatus and breath gases were collected and analyzed during 3 days of each 9-day metabolic period. Responses to feeding xylan, pectin, cellulose and corn bran were compared to a fiber-free formula diet. Generally, hydrogen production increased throughout the day, whereas methane production remained more constant. Methane excretion was greater while consuming the xylan and pectin diets than while consuming the other diets. These two purified fibers also caused higher flatus volume, hydrogen and carbon dioxide excretion. Cellulose and corn bran generally resulted in breath and flatus gas excretion at levels equivalent to fiber-free diets. Considerable variation was noted in the response of subjects to an individual diet. However, in most cases 2-5 days of frequent and daily consumption of the diets was necessary to establish a relatively constant level of gas excretion. This time may represent the period of microbial and enzymatic adaptation to the new dietary constituents.

[mle_ii]

Inhibition of Methanogenisis:
Inhibition of methanogenesis by human bile.
http://www.ncbi.nlm.nih.gov/sites/entre ... ds=7590441
http://gut.bmj.com/cgi/reprint/37/3/418

Gut. 1995 Sep;37(3):418-21
The factors that regulate methanogenesis in humans have not been established. The presence of bile acid, which is lost into the colon from the small intestine, may be an important regulatory factor of methanogenesis. To examine this possibility, the effect of human bile on methane production by faecal cultures, and the in vivo effect of biliary diversion on breath methane excretion in a methanogenic choledochostomy patient, were investigated. Faecal suspensions (0.1%) from five methanogenic humans were incubated anaerobically with bile (0.3-30%) from three choledochostomy patients, and headspace methane measured by gas chromatography. All biles inhibited headspace methane. Inhibition of methanogenesis was dose dependent, plateaued at 10-30% bile concentration, and was abolished by 0.6% cholestyramine. The maximum inhibition by bile, median (range), was 38 (0.9-56)% of control methane values. Reversal of the bile fistula in the fourth choledochostomy patient converted that subject from methanogenic to 'non-methanogenic' status, It is concluded that inhibition of methanogens in the caecum by bile acid could significantly reduce the number of methanogens in the colon. This and the effect of transit time could explain much of the known epidemiology of 'non-methanogenesis', which has been related to obesity, (comparatively) fast colonic transit in healthy persons, and to small intestinal Crohn's disease.

A possible role for bile acid in the control of methanogenesis and the accumulation of hydrogen gas in the human colon.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=8003641

J Gastroenterol Hepatol. 1994 Mar-Apr;9(2):112-7
This study investigated a possible role for primary bile acid in the control of methanogenesis in the human colon. Production of hydrogen and methane was measured in anaerobic faecal cultures derived from faeces of six 'non-methanogenic' and three methanogenic healthy humans. Using a sensitive technique for gas measurement, methane was detected in all faecal cultures, including those from 'non-methanogenic' humans. Bile acid inhibited methanogenesis in a dose-response fashion in the in vitro 'non-methanogenic' and methanogenic faecal cultures. Inhibition was significant at bile acid concentrations > 0.05%. Methanogenesis correlated with methanogen (methanogenic bacteria) numbers. If this inhibition occurs in vivo, then it would explain much of the epidemiology of non-methanogenesis in humans. From an analysis of net hydrogen production by the faecal cultures, it is inferred that bile acid inhibits other hydrogen-consuming bacteria in addition to methanogens. These in vitro data suggest a major role for bile acid in the accumulation of hydrogen gas in the colon. Possible links between bile acid induced accumulation of gas and irritable bowel syndrome are discussed.

[mle_ii]

More random stuff to ignore. :)

Stuff for regulation of Migrating motor complex. More specifically Phase III, the cleansing phase. Disregulation of this can lead to bacterial overgrowth.

http://en.wikipedia.org/wiki/Migrating_Motor_Complex

Drugs:
Erythromycin
http://en.wikipedia.org/wiki/Motilin
http://en.wikipedia.org/wiki/Erythromycin
Morphine - Inhibits?


Hormones:
Motilin
Ghrelin
Serotonin - inhibits?
corticotropin-releasing factor (CRF) - Inhibits


Ginger: Induces
Effects of ginger on gastroduodenal motility.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=10442508

Acidity: Low Ph inhibits, high Ph induces?
Intragastric acidification inhibits motilin-induced phase III activity in humans.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=16918728
Duodenal pH governs interdigestive motility in humans.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=7840198

Synbiotics:
Relationship between dietary-induced changes in intestinal commensal microflora and duodenojejunal myoelectric activity monitored by radiotelemetry in the rat in vivo.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=16263800

Ghrelin:
Influence of ghrelin on interdigestive gastrointestinal motility in humans.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=16216827

Accupressure:
Effects of acupressure on gastric myoelectrical activity in healthy humans.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=15934175
http://www.acupuncture-acupressure-poin ... nt-P6.html
http://www.homebackpainacupressure.com/ ... kness.html

Motilin:
High interdigestive and postprandial motilin levels in patients with the irritable bowel syndrome.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=15670264

pancreatic enzymes:
Impaired gastric myoelectricity in patients with chronic pancreatitis: role of maldigestion.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=15637747

Erythromycin: Induces
Altered migrating myoelectrical complex in an animal model of cholesterol gallstone disease: the effect of erythromycin.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=9824610
Effects of oral erythromycin on fasting and postprandial antroduodenal motility in patients with type I diabetes, measured with an ambulatory manometric technique.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=9118759
Erythromycin induces migrating motor complex in human gastrointestinal tract.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=3943442

Clarithromycin: Induces
Dose-related stimulatory effect of clarithromycin on interdigestive gastroduodenal motility.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=10899723

Serotonin intravenous: Induces
Concentration-dependent stimulation of intestinal phase III of migrating motor complex by circulating serotonin in humans.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=9854466

Serotonin Reuptake Inhibitor: (SSRI) promotes
5-Hydroxytryptamine and human small intestinal motility: effect of inhibiting 5-hydroxytryptamine reuptake.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=8174987

Alcohol: Induces?
Effect of alcohol upon myoelectric activity of the gastrointestinal tract and pancreatic and biliary duct pressures.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=4002109



Dietary Cholesterol (high) inhibits?
Changes of gastrointestinal myoelectric activity and bile acid pool during cholesterol gallstone formation in guinea pig.http://www.cmj.org/Periodical/paperlist ... ype=pubmed

Bile Acid:
Effect of SC-435 on the gastrointestinal migrating myoelectric complex in guinea pigs.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=16320575

Bile acid Recirculation:
Relationship between entero-hepatic bile acid circulation and interdigestive migrating myoelectrical activity in rats.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=16149150

Nitric Oxide: inhibits
Endogenous nitric oxide modulates small intestinal nutrient transit and activity in healthy adult humans.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=16334438

Sildenafil: inhibits (Viagra)
Sildenafil inhibits gastroduodenal motility.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=11148432


Opoids: Inhibit? Not so sure as other studies seem to imply that it promotes phase III. Need to look more.
Different endogenous opioid effects on delta- and mu-receptor subtypes in antral and duodenal motility of conscious dogs.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=12018898




Stress: inhibits
Inhibitory effects of stress on postprandial gastric myoelectrical activity and vagal tone in healthy subjects.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=15601423

Travel Stress: inhibits
Travel stress alters the intestinal migrating myoelectric complex in rats: antagonist effect of trimebutine.
http://www.ncbi.nlm.nih.gov/sites/entre ... ch=1732698

Peppermint Oil and caraway oil: inhibits
Effects of intraduodenal application of peppermint oil (WS(R) 1340) and caraway oil (WS(R) 1520) on gastroduodenal motility in healthy volunteers.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=12601675

IBS, Bacterial overgrowth, MMC inhibited.
Lower frequency of MMC is found in IBS subjects with abnormal lactulose breath test, suggesting bacterial overgrowth.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=12498278
http://www.springerlink.com/content/r2n ... lltext.pdf

Total parenteral nutrition: Inhibits
Motility of the gastrointestinal tract and gallbladder during long-term total parenteral nutrition in dogs.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=12005462

[mle_ii]

Endorphines increased by
Alcohol
Cigerette smoking
Exercise
Chocolate
Low dose Naltrexone

Naltrexone and the immune system

The opioid antagonist naltrexone blocks acute endotoxic shock by inhibiting tumor necrosis factor-alpha production.
http://www.ncbi.nlm.nih.gov/pubmed/15265541

Opioid antagonist naltrexone disrupts feedback interaction between mu and delta opioid receptors in splenocytes to prevent alcohol inhibition of NK cell function.
http://www.ncbi.nlm.nih.gov/pubmed/15210757