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Crohn's Disease Forum » Books, Multimedia, Research & News » Etiology of inflammatory bowel disease: A unified hypothesis


 
01-22-2014, 10:23 AM   #301
kiny
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Looking back human history, when had people respected new theory? Are these important?
How do you explain people with diabetes who consume lots of saccharin, having low crohn's disease rates.

The American Diabetic Association has recommended saccharin for years, and yet these people have low rates of crohn's disease.
01-22-2014, 04:36 PM   #302
Xiaofa Qin
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How do you explain people with diabetes who consume lots of saccharin, having low crohn's disease rates.

The American Diabetic Association has recommended saccharin for years, and yet these people have low rates of crohn's disease.
As discussed in my early post (#148), to my knowledge, multiple studies back to 1980s found increased intake of refined sugar in patients with Crohn’s disease (here are some of the studies). However, the enthusiasm receded when some controlled trials failed to show a benefic with the restricted use of sugar (Ritchie JK, et al. Controlled multicentre therapeutic trial of an unrefined carbohydrate, fibre rich diet in Crohn's disease. Br Med J (Clin Res Ed). 1987 Aug 29;295(6597):517-20), especially the poor correlation between the Crohn’s disease and refined sugar consumption (Sonnenberg A. Geographic and temporal variations of sugar and margarine consumption in relation to Crohn's disease. Digestion. 1988;41(3):161-71 ). I suspected that this increased risk in IBD may relate to increased intake of artificial sweeteners rather than refined sugar. As patients with diabetes may have increased intake of sweeteners, I have tried to find if there is a link between diabetes and IBD. I indeed found some studies such as those showing an increased prevalence of diabetes in patients with ulcerative colitis (Kappelman MD, et al. Association of paediatric inflammatory bowel disease with other immune-mediated diseases. Arch Dis Child. 2011 Nov;96(11):1042-6) and a positive association between type 1 diabetes and Crohn’s disease in families (Sipetić S, et al. Family history and risk of type 1 diabetes mellitus. Acta Diabetol. 2002 Sep;39(3):111-5). I have not seen a study showing a reverse relationship between diabetes and CD, and would be happy to see the data you have.
01-22-2014, 04:41 PM   #303
durwardian
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Look instead at what the bugs feed off of, and each individuals intestinal flora balance

01-22-2014, 04:42 PM   #304
durwardian
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The more out of balance, and flattened, the harder it is to even absorb medicine or nuutrients

01-22-2014, 04:44 PM   #305
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So each case becomes a measure of poisons, toxins, diet, ability to absorb, actual bugs or bacteria present, state of the intestines, allergies, immune system, etc

01-22-2014, 04:46 PM   #306
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The causes are obviously, genetic, environmental, diet, and bugs, all different, but with similar results

01-24-2014, 06:58 AM   #307
mf15
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Can anyone get the full paper on this so we can figure out exactly what they are saying here,this one is a few days old.
Old Mike






Curr Opin Gastroenterol. 2014 Jan 16. [Epub ahead of print]

Proteases and small intestinal barrier function in health and disease.

Giuffrida P, Biancheri P, Macdonald TT.



Author information



Abstract

PURPOSE OF REVIEW:

To summarize the recent knowledge regarding intestinal proteases and the gut barrier.

RECENT FINDINGS:

It is now well established that intestinal proteases, such as matrix metalloproteinase (MMP)-1, MMP-3, MMP-10 and MMP-12, are key players in the development of ulcers in inflammatory bowel disease, have direct effects on epithelial barrier function and are involved in epithelial restitution. However, more recent work has suggested that the membrane-anchored epithelial cell serine protease matriptase is critical in maintaining the gut barrier, and roles have also been described for elastase, MMP-13, gelatinases, mast cell proteases and proteases derived from parasites and gut bacteria. Interestingly, epithelial proteases often co-localize with epithelial adherens junctions, and nonepithelial-derived proteases have junctional proteins as targets.

SUMMARY:

The role of proteases in controlling normal barrier function in the gut is now becoming very clear, to go alongside their role in intestinal inflammation.
01-24-2014, 11:01 AM   #308
wildbill_52280
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As discussed in my early post (#148), to my knowledge, multiple studies back to 1980s found increased intake of refined sugar in patients with Crohn’s disease (here are some of the studies). However, the enthusiasm receded when some controlled trials failed to show a benefic with the restricted use of sugar (Ritchie JK, et al. Controlled multicentre therapeutic trial of an unrefined carbohydrate, fibre rich diet in Crohn's disease. Br Med J (Clin Res Ed). 1987 Aug 29;295(6597):517-20), especially the poor correlation between the Crohn’s disease and refined sugar consumption (Sonnenberg A. Geographic and temporal variations of sugar and margarine consumption in relation to Crohn's disease. Digestion. 1988;41(3):161-71 ). I suspected that this increased risk in IBD may relate to increased intake of artificial sweeteners rather than refined sugar. As patients with diabetes may have increased intake of sweeteners, I have tried to find if there is a link between diabetes and IBD. I indeed found some studies such as those showing an increased prevalence of diabetes in patients with ulcerative colitis (Kappelman MD, et al. Association of paediatric inflammatory bowel disease with other immune-mediated diseases. Arch Dis Child. 2011 Nov;96(11):1042-6) and a positive association between type 1 diabetes and Crohn’s disease in families (Sipetić S, et al. Family history and risk of type 1 diabetes mellitus. Acta Diabetol. 2002 Sep;39(3):111-5). I have not seen a study showing a reverse relationship between diabetes and CD, and would be happy to see the data you have.
Xiaofa Qin, i mentioned this study earlier but perhaps you never got around to looking at it, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1247426/

but it did find a difference between sugar intake and fiber intake and benefits to crohns disease while following patients over the course of 4 years, contrary to the other study. i find that reducing my sugar intake to almost nothing has been one of the main principles that has eliminated diarhea symptoms, but not inflammation. i reduced not only refined sugar, but sugar that is naturally present in foods as well. and whenever i increase the sugar, diarhea can be brought right back, so the connection is irrefutable, many enterobacteria have what is called the lac operon, which enables them to utilize lactose as a food or to create metabolic by products. i have also followed a high fibre diet and have never been to the hospital in 4.5 years since being diagnosed.
01-24-2014, 02:11 PM   #309
Xiaofa Qin
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Can anyone get the full paper on this so we can figure out exactly what they are saying here,this one is a few days old.
Old Mike


Curr Opin Gastroenterol. 2014 Jan 16. [Epub ahead of print]

Proteases and small intestinal barrier function in health and disease.

Giuffrida P, Biancheri P, Macdonald TT.
I would like to help. However, my support as a researcher in the medical school was ended by the end of last year. Now I am staying at home and also cannot get the full text.

This may not be a bad thing. I also lost my job in 2001 that had given me the chance and time to learn more and get involved in IBD. As a spare time IBD researcher during the last decade, I believe I may made more progress toward a better understanding and final solution of IBD than the many studies supported by hundreds of millions or even billions of funding.

Staying at home, I have a vivid feeling of the real world, not just bubble and fantasy.

I can generate hypothesis and express my opinions through the literature. However, test of these hypotheses would need the field work. Before I have to find another job with IBD remaining a spare time hobby, if possible, I would like to use this opportunity to make a transition to become a full time IBD warrior – finding out the principle culprits in IBD that I believe could be just a few factors in the environment, and a cure for IBD that I believe the effective protection and fortification of gut barrier would be essential. Hope I may have the chance to do so. If anybody interested, please join the fight.
01-24-2014, 02:29 PM   #310
Xiaofa Qin
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Xiaofa Qin, i mentioned this study earlier but perhaps you never got around to looking at it, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1247426/

but it did find a difference between sugar intake and fiber intake and benefits to crohns disease while following patients over the course of 4 years, contrary to the other study.
The paper you cited above seems just the one I was cited in my post (#305)(Ritchie JK, et al. Controlled multicentre therapeutic trial of an unrefined carbohydrate, fibre rich diet in Crohn's disease. Br Med J (Clin Res Ed). 1987 Aug 29;295(6597):517-20), with the conclusion that "No clear difference in clinical course was detected among patients who accepted the two different types of dietary advice". Do you mean you have another paper?
01-24-2014, 07:20 PM   #311
wildbill_52280
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The paper you cited above seems just the one I was cited in my post (#305)(Ritchie JK, et al. Controlled multicentre therapeutic trial of an unrefined carbohydrate, fibre rich diet in Crohn's disease. Br Med J (Clin Res Ed). 1987 Aug 29;295(6597):517-20), with the conclusion that "No clear difference in clinical course was detected among patients who accepted the two different types of dietary advice". Do you mean you have another paper?
wow, so sorry, i put the wrong link in there. here is the other study i was talking about.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1596427/

There was 32 patients in the control group and 34 in the diet treated group, so its small, but found good results. i wonder if, or why wouldnt their have been larger studies confirming the role of this diet to manage crohns disease in addition to meds. its amazing what information there is out there when you actually look for it, thank god for the internet and free information. to reduce the amount of time spent in the hospital by 75%, that would save alot of money treating this disease, or to the contrary, profiteers from making money off this disease.




Treatment of Crohn's disease with an unrefined-carbohydrate, fibre-rich diet.

Br Med J. 1979 September 29; 2(6193): 764–766.
PMCID: PMC1596427
K W Heaton, J R Thornton, and P M Emmett

Abstract

Thirty-two patients with Crohn's disease were treated with a fibre-rich, unrefined-carbohydrate diet in addition to conventional management and followed for a mean of four years and four months. Their clinical course was compared retrospectively with that of 32 matched patients who had received no dietary instruction. Hospital admissions were significantly fewer and shorter in the diet-treated patients, who spent a total of 111 days in hospital compared with 533 days in the non-diet-treated control group. Whereas five of the controls required intestinal operation, only one diet-treated patient needed surgery. This is in strong contrast to general experience with this disease. Treatment with a fibre-rich, unrefined-carbohydrate diet appears to have a favourable effect on the course of Crohn's disease and does not lead to intestinal obstruction.
01-24-2014, 09:00 PM   #312
Xiaofa Qin
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wow, so sorry, i put the wrong link in there. here is the other study i was talking about.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1596427/

There was 32 patients in the control group and 34 in the diet treated group, so its small, but found good results. i wonder if, or why wouldnt their have been larger studies confirming the role of this diet to manage crohns disease in addition to meds. its amazing what information there is out there when you actually look for it, thank god for the internet and free information. to reduce the amount of time spent in the hospital by 75%, that would save alot of money treating this disease, or to the contrary, profiteers from making money off this disease.
Thanks for sharing the paper. Here again we can see the conflict results among the different studies.

Reading through the full text of these papers, we can found that the paper I cited (Ritchie JK, et al. Controlled multicentre therapeutic trial of an unrefined carbohydrate, fibre rich diet in Crohn's disease. Br Med J (Clin Res Ed). 1987 Aug 29;295(6597):517-20) was in fact just the larger study aimed at confirming the findings in the retrospective study you referred to, through a larger-scale, randomised prospective single blind trial. Unfortunately, it failed to repeat the beneficial effect of the unrefined-carbohydrate diet. Here is the link to the full text.
01-25-2014, 01:37 AM   #313
wildbill_52280
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Thanks for sharing the paper. Here again we can see the conflict results among the different studies.

Reading through the full text of these papers, we can found that the paper I cited (Ritchie JK, et al. Controlled multicentre therapeutic trial of an unrefined carbohydrate, fibre rich diet in Crohn's disease. Br Med J (Clin Res Ed). 1987 Aug 29;295(6597):517-20) was in fact just the larger study aimed at confirming the findings in the retrospective study you referred to, through a larger-scale, randomised prospective single blind trial. Unfortunately, it failed to repeat the beneficial effect of the unrefined-carbohydrate diet. Here is the link to the full text.

very interesting indeed. the second study was 2 years and the first was 4 years? didnt seem like the exact replication then, but im not really refuting their findings too much here though. I'll stick with the specificity of how my disease works, rather then enumerative induction(if 20 crohn's patients react the same way, then all must react this way), WHICH is unfortunatly how science is done. its possible some patients are more sensitive to these dietary factors then others which might explain the differences in findings.

Last edited by wildbill_52280; 01-25-2014 at 02:05 AM.
01-25-2014, 01:41 AM   #314
wildbill_52280
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I would like to help. However, my support as a researcher in the medical school was ended by the end of last year. Now I am staying at home and also cannot get the full text.

This may not be a bad thing. I also lost my job in 2001 that had given me the chance and time to learn more and get involved in IBD. As a spare time IBD researcher during the last decade, I believe I may made more progress toward a better understanding and final solution of IBD than the many studies supported by hundreds of millions or even billions of funding.

Staying at home, I have a vivid feeling of the real world, not just bubble and fantasy.

I can generate hypothesis and express my opinions through the literature. However, test of these hypotheses would need the field work. Before I have to find another job with IBD remaining a spare time hobby, if possible, I would like to use this opportunity to make a transition to become a full time IBD warrior – finding out the principle culprits in IBD that I believe could be just a few factors in the environment, and a cure for IBD that I believe the effective protection and fortification of gut barrier would be essential. Hope I may have the chance to do so. If anybody interested, please join the fight.
of course my opinoin isnt very well developed yet, but take another look at soy products. i have some interesting studies ill send your way. this is based on using myself, my own testimony/experiance of having IBD a as source of clues. in 2006-7 i stopped drinking milk and switched entirely to drinking silk soy milk which has carageenen and trypsin inhibitors, i learned weeks ago of the possibility that trypsin is a requirement for the production of defensins, which vitamin d is also a requirement to make defensins, possibly bringing the information we have on north south gradient of ibd incidence and how low vitamin d may protect from dysbiosis, soy products may have a similar damaging effect increasing risk of ibd. The main variable i believe caused crohn's was amoxicillin, but the soy milk may have put me at greater risk. i believe i developed it in feb 2008 after antibiotics, diagnosed april 2009.

the presence of active trypsin is needed for maximum production of defensins in the lining of the gut, or at least maybe. it may take alot of soy mlik to depress enough defensins to create ibd though, some things to look into.

Last edited by wildbill_52280; 01-25-2014 at 02:10 AM.
01-25-2014, 09:47 AM   #315
Xiaofa Qin
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of course my opinoin isnt very well developed yet, but take another look at soy products. i have some interesting studies ill send your way. this is based on using myself, my own testimony/experiance of having IBD a as source of clues. in 2006-7 i stopped drinking milk and switched entirely to drinking silk soy milk which has carageenen and trypsin inhibitors, i learned weeks ago of the possibility that trypsin is a requirement for the production of defensins, which vitamin d is also a requirement to make defensins, possibly bringing the information we have on north south gradient of ibd incidence and how low vitamin d may protect from dysbiosis, soy products may have a similar damaging effect increasing risk of ibd. The main variable i believe caused crohn's was amoxicillin, but the soy milk may have put me at greater risk. i believe i developed it in feb 2008 after antibiotics, diagnosed april 2009.

the presence of active trypsin is needed for maximum production of defensins in the lining of the gut, or at least maybe. it may take alot of soy mlik to depress enough defensins to create ibd though, some things to look into.
The body is complex. The world is complex. Trypsin may indeed stimulate the production of defensins that are regarded as important protective molecules for the gut. However, it has been well documented that treatment with antibiotics will result in a dramatic increase of digestive proteases like trypsin in the lower gut due to impaired inactivation, thus, according to your info, this may lead to great increase in the production of defensins. However, antibiotics increased but not decreased the risk of IBD. So, is increased trypsin really beneficial or actually detrimental? Is the inhibition of trypsin by some components in the soy milk more likely increased or decreased the risk of IBD? We may have to make a comprehensive analysis of the different evidences, most times being conflicting, rather than a piece of evidence, to get a likely right judgment.
01-25-2014, 12:36 PM   #316
wildbill_52280
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The body is complex. The world is complex. Trypsin may indeed stimulate the production of defensins that are regarded as important protective molecules for the gut. However, it has been well documented that treatment with antibiotics will result in a dramatic increase of digestive proteases like trypsin in the lower gut due to impaired inactivation, thus, according to your info, this may lead to great increase in the production of defensins. However, antibiotics increased but not decreased the risk of IBD. So, is increased trypsin really beneficial or actually detrimental? Is the inhibition of trypsin by some components in the soy milk more likely increased or decreased the risk of IBD? We may have to make a comprehensive analysis of the different evidences, most times being conflicting, rather than a piece of evidence, to get a likely right judgment.
good points, i agree, the impact of trypsin inhibitors from soy milk, may be so miniscule. ill send some links anyway, its interesting stuff either way.


Trypsin Mediates Growth Phase-Dependent Transcriptional Regulation of Genes Involved in Biosynthesis of Ruminococcin A, a Lantibiotic Produced by a Ruminococcus gnavus Strain from a Human Intestinal Microbiota

ABSTRACT
Ruminococcin A (RumA) is a trypsin-dependent l antibiotic produced byRuminococcus gnavus E1, a gram-positive strict anaerobic strain isolated from a human intestinal microbiota. A 12.8-kb region from R. gnavus E1 chromosome, containing the biosynthetic gene cluster of RumA, has been cloned and sequenced. It consisted of 13 open reading frames, organized in three operons with predicted functions in lantibiotic biosynthesis, signal transduction regulation, and immunity. One unusual feature of the locus is the presence of three almost identical structural genes, all of them encoding the RumA precursor. In order to determine the role of trypsin in RumA production, the transcription of the rum genes has been investigated under inducing and noninducing conditions. Trypsin activity is needed for the growth phase-dependent transcriptional activation of RumA operons. Our results suggest that bacteriocin production by R. gnavus E1 is controlled through a complex signaling mechanism involving the proteolytic processing of a putative extracellular inducer-peptide by trypsin, a specific environmental cue of the digestive ecosystem.

link: http://jb.asm.org/content/184/1/18.full




Biologically-active defensins are released upon the proteolytic processing of their proforms by certain enzymes[4], including trypsin for DEFA5 and DEFA6 in humans[5] and matrilysin for cryptdins in mice[6]. This suggests that appropriate control of homeostatic quantities of both defensins and defensin-activating proteases may ultimately dictate the outcome of the gut immunological response to intruding pathogens and to commensal microorganisms that are permanently present.
source: http://www.wjgnet.com/1007-9327/full/v17/i5/567.htm
01-25-2014, 12:55 PM   #317
Xiaofa Qin
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Thank you wildbill for sharing the paper. Here is a study showing that trypsin in fecal extracts may increase 100 times after the treatment by antibiotics.

-----------------

Digestion. 1983;27(1):8-15.

Determination of immunoreactive trypsin, pancreatic elastase and chymotrypsin in extracts of human feces and ileostomy drainage.

Bohe M, Borgström A, Genell S, Ohlsson K.

Abstract

The total daily amount of extractable cationic trypsin, chymotrypsin, and pancreatic elastase 2 in feces and ileostomy fluids has been studied in normal individuals and healthy colectomized subjects. Quantitation was performed using immunological assays with polyethylene glycol as a fecal marker. The extractable amount of each of these enzymes in the feces of normal individuals was less than 1 mg/24 h. However, in fecal extracts from antibiotic-treated normal individuals a 100-fold increase in immunoreactive cationic trypsin was observed, while chymotrypsin and elastase 2 were only 2- to 3-fold higher. In extracts from ileostomy fluids cationic trypsin, elastase, and chymotrypsin all showed mean values in the order of 50-200 mg/24 h. The characterization of the immunoreactivity of pancreatic proteases showed no qualitative differences when measured in duodenal juice or fecal and ileostomy extracts.


PMID: 6554206 [PubMed - indexed for MEDLINE]
01-25-2014, 03:07 PM   #318
wildbill_52280
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Thank you wildbill for sharing the paper. Here is a study showing that trypsin in fecal extracts may increase 100 times after the treatment by antibiotics.

-----------------

Digestion. 1983;27(1):8-15.

Determination of immunoreactive trypsin, pancreatic elastase and chymotrypsin in extracts of human feces and ileostomy drainage.

Bohe M, Borgström A, Genell S, Ohlsson K.

Abstract

The total daily amount of extractable cationic trypsin, chymotrypsin, and pancreatic elastase 2 in feces and ileostomy fluids has been studied in normal individuals and healthy colectomized subjects. Quantitation was performed using immunological assays with polyethylene glycol as a fecal marker. The extractable amount of each of these enzymes in the feces of normal individuals was less than 1 mg/24 h. However, in fecal extracts from antibiotic-treated normal individuals a 100-fold increase in immunoreactive cationic trypsin was observed, while chymotrypsin and elastase 2 were only 2- to 3-fold higher. In extracts from ileostomy fluids cationic trypsin, elastase, and chymotrypsin all showed mean values in the order of 50-200 mg/24 h. The characterization of the immunoreactivity of pancreatic proteases showed no qualitative differences when measured in duodenal juice or fecal and ileostomy extracts.


PMID: 6554206 [PubMed - indexed for MEDLINE]

thanks. maybe this slightly suggests trypsin inhibition would not be enough to deplete defensins and affect dysbiosis leading to IBD. but it could also suggest increases in trypsin production are a compensatory defense mechanism to also increase defensin to counteract the dysbiosis induced by antibiotics.

i'm still not sure that is enough to prove that trypsin inhibitors do not affect defensin production.

the question remains:
do trypsin inhibitors from soy products specifically in soy milk, in any quantity, affect defensin production. i suppose then that is my question.
01-25-2014, 03:13 PM   #319
wildbill_52280
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here is some info on the production of soy milk and trypsin inhibitor content:

J Agric Food Chem. 2008 Sep 10;56(17):7957-63. doi: 10.1021/jf801039h. Epub 2008 Aug 9.

Elimination of trypsin inhibitor activity and beany flavor in soy milk by consecutive blanching and ultrahigh-temperature (UHT) processing.


Abstract

Soy foods contain significant health-promoting components but also may contain beany flavor and trypsin inhibitor activity (TIA), which can cause pancreatic disease if present at a high level. Thermal processing can inactivate TIA and lipoxygenase. Ultrahigh-temperature (UHT) processing is relatively new for manufacturing soy milk. Simultaneous elimination of TIA and soy odor by UHT processing for enhancing soy milk quality has not been reported. The objective was to determine TIA in soy milk processed by traditional, steam injection, blanching, and UHT methods and to compare the products with commercial soy milk products. Soybean was soaked and blanched at 70-85 degrees C for 30 s-7.5 min. The blanched beans were made into base soy milk. The hexanal content of the base soy milk was determined by gas chromatography to determine the best conditions for further thermal processing by indirect and direct UHT methods at 135-150 degrees C for 10-50 s using the Microthermics processor. Soy milk was also made from soaked soybeans by traditional batch cooking and steaming methods. Eighteen commercial products were selected from the supermarket. Residual TIA in soy milk processed by the traditional and steam injection to 100 degrees C for 20 min was approximately 13%. Blanching could inactivate 25-50% of TIAs of the raw soy milk. The blanch conditions of 80 degrees C and 2 min were selected for UHT processing because these conditions produced blanched soy milk without hexanal, indicating a complete heat inactivation of lipoxygenases. The TIA decreased with increased temperature and time of UHT heating. The maximal trypsin inhibitor inactivation was achieved by UHT direct and indirect methods with residual activities of approximately 10%. Some commercial soy milk products contained high TIAs (trypsin inhibitor activity). The results are important to the food industry and consumers. Kinetic analysis showed that heat inactivation (denaturation) of TIA, under the continuous processing conditions of the Microthermics processor, followed first-order reaction kinetics, and the activation energy of the inactivation was 34 kJ/mol.
01-25-2014, 08:42 PM   #320
durwardian
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What about these trials? What does this tell us about what is going on in the gut?
http://www.medicalnewstoday.com/articles/249497.php

01-25-2014, 08:46 PM   #321
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Could it be that these parasites are killing off the competition before they perish? Not that the immune system is "BOOSTED" or "CORRECTED"

01-25-2014, 08:48 PM   #322
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The boost comes when the body is no longer fighting? And that the lack of ability to produce proper pancreatic balance is the root cause?

01-25-2014, 09:08 PM   #323
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the pig parasite trials unfortunately came back as ineffective
01-25-2014, 09:24 PM   #324
durwardian
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I am willing to bet they work in a certain type of bowel disease, hopefully they aren't tossing the soup for lack of salt?

01-25-2014, 09:25 PM   #325
durwardian
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Which would prove my point that Crohn's isn't always the same disease, it is a bunch of different ones with similar symptoms

01-25-2014, 09:35 PM   #326
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that seems to be the problem with most trials, they need to look at ALL the variables, I.e did the people that showed response have certain characteristics, i.e granuloma formation, or no granuloma, disease location etc, atm I think everything is too broadly looked at. I don't have the link to the results of the trials but they're somewhere on here, I remember it not being any higher than the placebo control though...
01-26-2014, 01:01 AM   #327
durwardian
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And if an immune response showed promise, what other ways can that be triggered?

01-26-2014, 04:02 AM   #328
durwardian
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The goal would be a cure, which could end up being genetic reprogramming. I have also heard of healthy family members donating healthy intestinal flora for an infusion into the afflicted's bowels.

01-26-2014, 04:03 AM   #329
durwardian
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Like the body needs a reminder, it appears to work to restore balance?

01-26-2014, 10:27 AM   #330
wildbill_52280
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The goal would be a cure, which could end up being genetic reprogramming. I have also heard of healthy family members donating healthy intestinal flora for an infusion into the afflicted's bowels.
thats called a fecal microbiota transplant.

- http://www.crohnsforum.com/showthread.php?t=52400
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