https://www.sciencedaily.com/releases/2 ... 150622.htm
Saw this this morning just wanted to share if you haven't seen it yet....
New Study Out
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
New Study Out
Martha E.
Philippians 4:13
Jul 2008 took Clindamycin for a Sinus infection that forever changed my life
Dec 2014 MC Dx
Jul 15, 2015 Elimination Diet
Aug 17, 2015 Enterolab Test
Dec 2015 Reflux
Sept 2016 IC
Philippians 4:13
Jul 2008 took Clindamycin for a Sinus infection that forever changed my life
Dec 2014 MC Dx
Jul 15, 2015 Elimination Diet
Aug 17, 2015 Enterolab Test
Dec 2015 Reflux
Sept 2016 IC
Hi Martha,
That's an interesting premise, but with all due respect to the authors/researchers, I believe they are .
Here's why. They make the initial assumption that IBDs are caused by the inability of the mucin glands in the crypts of our intestinal mucosa to produce mucin rapidly enough to prevent bacteria in the fecal stream from attacking the mucosa. (When mucin mixes with water, it produces mucus, which lubricates and protects the surface of the mucosa.)
It's an interesting theory, and for decades researchers have theorized that bacteria are the cause of IBDs, but so far no one has been able to demonstrate that bacteria are the cause of IBDs, let alone prove that the reason why bacteria are the cause of IBDs is because of compromised mucin production by our mucosa.
First off, without proof that bacteria are the cause of IBDs, any secondary conclusions based on that assumption are little more than speculative. And secondly, the assumption that compromised mucin production is implicated in the etiology of IBDs appears to be incorrect. As evidence, look at how many members here have posted about the extreme volume of mucus in their BMs when their MC is really flaring. I've experienced it, and probably you have also. If our crypt glands can't produce at least normal amounts of mucin, then where in the world does all that mucus come from when we are reacting? Has anyone who doesn't have an IBD ever reported such high volume of mucus production? I'll bet not. I've never heard of it. So I have to conclude that we (as IBD patients) are virtually all capable of producing more than adequate amounts of mucin/mucus.
And they also took extreme liberty by defining that gene as a "gene that protects against inflammatory bowel disease". They can't say that, not based on their research, because their research is based on an assumption, not fact. They have no proof that mucin protects against IBDs. All they know is that the gene affects the production of mucin. And their data suggested that genetic manipulation of mucin production in mice caused "symptoms similar to people with IBD". But that's a far cry from proving that genetic mucin manipulation in humans has anything to do with the etiology of IBD. According to the researchers:
Before any of this type of research means anything, I'd like to see some proof that bacteria cause IBDs.
That said, it's still progress, and it's always good to see what researchers are thinking, and their research may inspire someone else to design a research study that will be based on facts, rather than limited by assumptions.
Thanks for the link.
Tex
That's an interesting premise, but with all due respect to the authors/researchers, I believe they are .
Here's why. They make the initial assumption that IBDs are caused by the inability of the mucin glands in the crypts of our intestinal mucosa to produce mucin rapidly enough to prevent bacteria in the fecal stream from attacking the mucosa. (When mucin mixes with water, it produces mucus, which lubricates and protects the surface of the mucosa.)
It's an interesting theory, and for decades researchers have theorized that bacteria are the cause of IBDs, but so far no one has been able to demonstrate that bacteria are the cause of IBDs, let alone prove that the reason why bacteria are the cause of IBDs is because of compromised mucin production by our mucosa.
First off, without proof that bacteria are the cause of IBDs, any secondary conclusions based on that assumption are little more than speculative. And secondly, the assumption that compromised mucin production is implicated in the etiology of IBDs appears to be incorrect. As evidence, look at how many members here have posted about the extreme volume of mucus in their BMs when their MC is really flaring. I've experienced it, and probably you have also. If our crypt glands can't produce at least normal amounts of mucin, then where in the world does all that mucus come from when we are reacting? Has anyone who doesn't have an IBD ever reported such high volume of mucus production? I'll bet not. I've never heard of it. So I have to conclude that we (as IBD patients) are virtually all capable of producing more than adequate amounts of mucin/mucus.
And they also took extreme liberty by defining that gene as a "gene that protects against inflammatory bowel disease". They can't say that, not based on their research, because their research is based on an assumption, not fact. They have no proof that mucin protects against IBDs. All they know is that the gene affects the production of mucin. And their data suggested that genetic manipulation of mucin production in mice caused "symptoms similar to people with IBD". But that's a far cry from proving that genetic mucin manipulation in humans has anything to do with the etiology of IBD. According to the researchers:
"This gene and others?" "May account for some cases of IBD in hymans". That's mighty speculative, but I will agree that it might be a factor in a limited number of cases. The problem is that the article headline makes it sound as though they've discovered the key to the cause of IBD and they obviously have not."Mutations in this gene and others needed for mobilization of energy in cells may account for some cases of IBD in humans," said Dr. Beutler, also Professor of Immunology.
Before any of this type of research means anything, I'd like to see some proof that bacteria cause IBDs.
That said, it's still progress, and it's always good to see what researchers are thinking, and their research may inspire someone else to design a research study that will be based on facts, rather than limited by assumptions.
Thanks for the link.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Dang Tex! What you are saying definitely makes since....I was so hoping they were getting closer!
Martha E.
Philippians 4:13
Jul 2008 took Clindamycin for a Sinus infection that forever changed my life
Dec 2014 MC Dx
Jul 15, 2015 Elimination Diet
Aug 17, 2015 Enterolab Test
Dec 2015 Reflux
Sept 2016 IC
Philippians 4:13
Jul 2008 took Clindamycin for a Sinus infection that forever changed my life
Dec 2014 MC Dx
Jul 15, 2015 Elimination Diet
Aug 17, 2015 Enterolab Test
Dec 2015 Reflux
Sept 2016 IC