Re: How ulcerative colitis works

[Guest guest]

Before I read this, does it say IBD is an infectious disease?

 

Thanks,

Debbie 40 cd

I was diagnosed with UC two years ago and ever since I wanted to learn as much as possible about the disease. I'm fortunate to have a sister that's a professor in nutrition and she directed me to a paper that gave an insight as to what might cause UC. I followed the author's work and found a nice summary here:

http://www.hsph.harvard.edu/news/hphr/infectious-diseases/infectious-diseases-bacteria-without-borders/index.html

I hope you find it interesting and learn something new about the inflammatory process related to UC.Please let me know if you know of other resources that list potential causes of IBD.

[Guest guest]

The authors are not suggesting that IBD is an infectious or communicable disease

in humans.

>

> >

> >

> > I was diagnosed with UC two years ago and ever since I wanted to learn as

> > much as possible about the disease. I'm fortunate to have a sister that's a

> > professor in nutrition and she directed me to a paper that gave an insight

> > as to what might cause UC. I followed the author's work and found a nice

> > summary here:

> >

> >

> >

http://www.hsph.harvard.edu/news/hphr/infectious-diseases/infectious-diseases-ba\

cteria-without-borders/index.html

> >

> > I hope you find it interesting and learn something new about the

> > inflammatory process related to UC.

> >

> > Please let me know if you know of other resources that list potential

> > causes of IBD.

> >

> >

> >

>

[Guest guest]

> The authors are not suggesting that IBD is an infectious or

> communicable disease in humans.

>

>

>>

>> Before I read this, does it say IBD is an infectious disease?

No, genetic. The genetic lack of an immune system protein.

This study came out a few years back and we discussed it at the time.

Very interesting study for those who haven't read it yet.

Mara

[Guest guest]

It says this:In a surprising discovery, HSPH immunologist Laurie Glimcher and postdoctoral fellow Garrett and their team have unmasked the immune peacekeeper in mice and showed how its absence triggers the inflammatory border conflict. What’s more, after finding that mice with ulcerative colitis can pass their disease on by transmitting gut bacteria, they cured those cases with standard antibiotics.

....Equally surprising was that diseased mice could transmit their illness to mice whose immune systems were normal, their T-bet function undisturbed. Successfully blocking transmission of their colitis with antibiotics proved that immune malfunction had led to the production of harmful bacteria and was indeed the key to this perplexing disease.

Before I read this, does it say IBD is an infectious disease?

 

Thanks,

Debbie 40 cd

I was diagnosed with UC two years ago and ever since I wanted to learn as much as possible about the disease. I'm fortunate to have a sister that's a professor in nutrition and she directed me to a paper that gave an insight as to what might cause UC. I followed the author's work and found a nice summary here:

http://www.hsph.harvard.edu/news/hphr/infectious-diseases/infectious-diseases-bacteria-without-borders/index.html

I hope you find it interesting and learn something new about the inflammatory process related to UC.Please let me know if you know of other resources that list potential causes of IBD.

[Guest guest]

There's more:

A communicable disease?It appears the T-bet protein’s job is to keep TNF-alpha in dendritic cells under control, to “maintain harmony between the host and bacteria in the gut,” Garrett explains. Lose T-bet, and bad things happen.

Without T-bet, the mix of intestinal bacteria appears to change, favoring dangerous pathogens, the investigators observed. A big surprise was that T-bet knockout mice in which ulcerative colitis developed passed the disease to offspring with normal T-bet levels, and even to unrelated healthy adult mice, presumably through oral-fecal contact.

The researchers didn’t know which types of bacteria were causing the colitis, but broad-spectrum antibiotics cured it.That the disease could be transmitted this way “is quite a striking finding,” Garrett says. “It’s amazing to us that the loss of an immune system protein in the host changes the mix of bacteria in the colon in a way that causes disease and drives colitis in healthy mice.”

That said, Garrett emphasizes, “We are not suggesting that inflammatory bowel disease is an infectious or communicable disease in humans.” Even in poor countries where fecal contamination of water is widespread, there is no evidence to suggest that the disease spreads between people.

Using their mouse model, the HSPH researchers showed that ulcerative colitis could be cured using antibodies that block TNF-alpha. Anti-TNF drugs are already used to treat inflammatory bowel disease, but the results and safety profile are far from ideal. Perhaps, Glimcher says, it might be possible to keep TNF-alpha under control by boosting T-bet in colonic dendritic cells. Another treatment strategy, one already used by some patients, is to consume “probiotic” foods, such as yogurt, to nurture the colonies of “good” bacteria that normally keep harmful microbes from getting out of hand.

It says this:In a surprising discovery, HSPH immunologist Laurie Glimcher and postdoctoral fellow Garrett and their team have unmasked the immune peacekeeper in mice and showed how its absence triggers the inflammatory border conflict. What’s more, after finding that mice with ulcerative colitis can pass their disease on by transmitting gut bacteria, they cured those cases with standard antibiotics.

....Equally surprising was that diseased mice could transmit their illness to mice whose immune systems were normal, their T-bet function undisturbed. Successfully blocking transmission of their colitis with antibiotics proved that immune malfunction had led to the production of harmful bacteria and was indeed the key to this perplexing disease.

Before I read this, does it say IBD is an infectious disease?

 

Thanks,

Debbie 40 cd

I was diagnosed with UC two years ago and ever since I wanted to learn as much as possible about the disease. I'm fortunate to have a sister that's a professor in nutrition and she directed me to a paper that gave an insight as to what might cause UC. I followed the author's work and found a nice summary here:

http://www.hsph.harvard.edu/news/hphr/infectious-diseases/infectious-diseases-bacteria-without-borders/index.html

I hope you find it interesting and learn something new about the inflammatory process related to UC.Please let me know if you know of other resources that list potential causes of IBD.

[Guest guest]

Based on this portion of the article:

> Using their mouse model, the HSPH researchers showed that ulcerative

colitis

> could be cured using antibodies that block TNF-alpha. Anti-TNF drugs

are

> already used to treat inflammatory bowel disease, but the results and

safety

> profile are far from ideal.

Isn't that what LDN does (block TNF-alpha)? Maybe that's why people are

having good luck with it. This is an interesting article.

Kathy

UC since 12/05

SCD since 7/07

[Guest guest]

Based on this portion of the article:

> Using their mouse model, the HSPH researchers showed that ulcerative

colitis

> could be cured using antibodies that block TNF-alpha. Anti-TNF drugs

are

> already used to treat inflammatory bowel disease, but the results and

safety

> profile are far from ideal.

Isn't that what LDN does (block TNF-alpha)? Maybe that's why people are

having good luck with it. This is an interesting article.

Kathy

UC since 12/05

SCD since 7/07

[Guest guest]

Based on this portion of the article:

> Using their mouse model, the HSPH researchers showed that ulcerative

colitis

> could be cured using antibodies that block TNF-alpha. Anti-TNF drugs

are

> already used to treat inflammatory bowel disease, but the results and

safety

> profile are far from ideal.

Isn't that what LDN does (block TNF-alpha)? Maybe that's why people are

having good luck with it. This is an interesting article.

Kathy

UC since 12/05

SCD since 7/07

[Guest guest]

No, genetic. The genetic lack of an immune system protein.Speaking of genetics and UC, my parents told me that when I was a baby, I had really bad colic, which has to do with your gut. Just wondering if there's any correlation, like what percentage of people with gut issues now had that when they were little...?Pour Dieu, pour terre,Alyssa =D

[Guest guest]

No, genetic. The genetic lack of an immune system protein.Speaking of genetics and UC, my parents told me that when I was a baby, I had really bad colic, which has to do with your gut. Just wondering if there's any correlation, like what percentage of people with gut issues now had that when they were little...?Pour Dieu, pour terre,Alyssa =D

[Guest guest]

No, genetic. The genetic lack of an immune system protein.Speaking of genetics and UC, my parents told me that when I was a baby, I had really bad colic, which has to do with your gut. Just wondering if there's any correlation, like what percentage of people with gut issues now had that when they were little...?Pour Dieu, pour terre,Alyssa =D

[Guest guest]

Hi Kathy,

No.. LDN does not do this at all.

I think you are confusing biological drugs like Remicade and Humira (which work

on an anti TNF basis) with Low Dose Naltrexone.

LDN works on a completely different level. It is way less harmful (I say way

less as IMO we still do not know long term effects as it is still a drug)

Jodi

> Isn't that what LDN does (block TNF-alpha)? Maybe that's why people are

> having good luck with it. This is an interesting article.

>

> Kathy

> UC since 12/05

> SCD since 7/07

>

[Guest guest]

Hi Kathy,

No.. LDN does not do this at all.

I think you are confusing biological drugs like Remicade and Humira (which work

on an anti TNF basis) with Low Dose Naltrexone.

LDN works on a completely different level. It is way less harmful (I say way

less as IMO we still do not know long term effects as it is still a drug)

Jodi

> Isn't that what LDN does (block TNF-alpha)? Maybe that's why people are

> having good luck with it. This is an interesting article.

>

> Kathy

> UC since 12/05

> SCD since 7/07

>

[Guest guest]

Hi Alyssa..

I had major colic and chronic ear infections as a baby too.

You will find that many of us IBD'ers have this in common.

Dr Natasha McBride wrote " Gut and Psychology Syndrome " she addresses

this a lot in her book- the idea that many of us IBD, ASD have gut dysbiosis

from an early age even in Utero as we can inherit our mothers gut dysbiosis.

According to her- things like antibiotics, birth control, diet and some other

factors are all reasons why we have bad gut ecology. The first place a newborn

comes into contact with " good bacteria " is in the vaginal canal. When a mother

has dysbiosis herself that infant already is in a disadvantage due to not

getting those good bacteria, so immune wise that infant is at a disadvantage

already. Not to mention how many c-section births there are today.

She says due to what I just stated and things like immunizations and many other

things we get show colic and ear issues. She claims that our eustchean (however

that is spelled) tubes are stuffed up. I totally agree to this.

I remember one day reaching a new level of health when my chiro adjusted my

eustachean tubes and all of this liquid started coming out. I wanted to keep

the liquid and put it on a Petri dish. perhaps ask AJ what the heck was inside

it. EWWW and fascinating at the same time.

So in summary, let's take our SCD probiotics and SCD ferments and get that

dysbiosis under control! Amen!

Jodi

[Guest guest]

Hi Alyssa..

I had major colic and chronic ear infections as a baby too.

You will find that many of us IBD'ers have this in common.

Dr Natasha McBride wrote " Gut and Psychology Syndrome " she addresses

this a lot in her book- the idea that many of us IBD, ASD have gut dysbiosis

from an early age even in Utero as we can inherit our mothers gut dysbiosis.

According to her- things like antibiotics, birth control, diet and some other

factors are all reasons why we have bad gut ecology. The first place a newborn

comes into contact with " good bacteria " is in the vaginal canal. When a mother

has dysbiosis herself that infant already is in a disadvantage due to not

getting those good bacteria, so immune wise that infant is at a disadvantage

already. Not to mention how many c-section births there are today.

She says due to what I just stated and things like immunizations and many other

things we get show colic and ear issues. She claims that our eustchean (however

that is spelled) tubes are stuffed up. I totally agree to this.

I remember one day reaching a new level of health when my chiro adjusted my

eustachean tubes and all of this liquid started coming out. I wanted to keep

the liquid and put it on a Petri dish. perhaps ask AJ what the heck was inside

it. EWWW and fascinating at the same time.

So in summary, let's take our SCD probiotics and SCD ferments and get that

dysbiosis under control! Amen!

Jodi

[Guest guest]

Hi Alyssa..

I had major colic and chronic ear infections as a baby too.

You will find that many of us IBD'ers have this in common.

Dr Natasha McBride wrote " Gut and Psychology Syndrome " she addresses

this a lot in her book- the idea that many of us IBD, ASD have gut dysbiosis

from an early age even in Utero as we can inherit our mothers gut dysbiosis.

According to her- things like antibiotics, birth control, diet and some other

factors are all reasons why we have bad gut ecology. The first place a newborn

comes into contact with " good bacteria " is in the vaginal canal. When a mother

has dysbiosis herself that infant already is in a disadvantage due to not

getting those good bacteria, so immune wise that infant is at a disadvantage

already. Not to mention how many c-section births there are today.

She says due to what I just stated and things like immunizations and many other

things we get show colic and ear issues. She claims that our eustchean (however

that is spelled) tubes are stuffed up. I totally agree to this.

I remember one day reaching a new level of health when my chiro adjusted my

eustachean tubes and all of this liquid started coming out. I wanted to keep

the liquid and put it on a Petri dish. perhaps ask AJ what the heck was inside

it. EWWW and fascinating at the same time.

So in summary, let's take our SCD probiotics and SCD ferments and get that

dysbiosis under control! Amen!

Jodi

[Guest guest]

I had major colic and chronic ear infections as a baby tooThe first place a newborn comes into contact with "good bacteria" is in the vaginal canal. No way!!! My mom would freak at hearing this. I had nonstop ear infections colic, hiccups (not sure that's related, but I had them and still do!) AND I was c-section!! It all makes sense now! (sort of). That's crazy! Pour Dieu, pour terre,Alyssa =D

[Guest guest]

Alyssa..

You gave me a good belly laugh..

Read the book.. It gives more insight into our mysterious condition. Not that

it has all the answers and NCM allowing bifidus for IBD'ers make more than my

brow raise.. But still she is incredibly insightful.

Jodi

[Guest guest]

FWIW...we were just having a discussion about this over on the pecanbread site.

My ASD daughter was an emergency c-section. My older daughter is not ASD, but

she was a very tough birth, and I found out after 2 weeks of nursing her that

she wasn't getting any milk from me. She has some weird things going on

digestive-wise, has eczema, etc.

I later connected the dots with my mom that I was on a bunch of antibiotics as a

kid, not to mention tetracycline and erethrimycin (no clue how to spell that!)

for acne as a teen. Add to that being on the pill later and that spelled

disaster for my kids.

I felt guilt for about 5 seconds then realized I have the chance to give my

daughters an incredible gift...heal their guts so they will not pass this

" vicious cycle " on to THEIR kids.

Kelley W.

>

> I had major colic and chronic ear infections as a baby too

>

> The first place a newborn comes into contact with " good bacteria " is

> in the vaginal canal.

>

> No way!!! My mom would freak at hearing this. I had nonstop ear

> infections colic, hiccups (not sure that's related, but I had them and

> still do!) AND I was c-section!! It all makes sense now! (sort of).

> That's crazy!

>

>

>

> Pour Dieu, pour terre,

> Alyssa =D

>

[Guest guest]

Alyssa..You gave me a good belly laugh..Read the book.. It gives more insight into our mysterious condition. Not that it has all the answers and NCM allowing bifidus for IBD'ers make more than my brow raise.. But still she is incredibly insightful.JodiGood, we all need one of those once in a while =) Do you think a library would have the book? If not I might just have to buy it =) Sounds like it's worth it though. Pour Dieu, pour terre,Alyssa =D

[Guest guest]

I was actually a pretty healthy kid, and was often one of a handful of kids in

my class who didn't come down with the flu. I've had one ear infection in my

whole life, and that was when I was 27 or so. I never had antibiotics until I

was 15 and had a sore throat that wouldn't go away. I only had them on one more

occasion prior to my Crohn's diagnosis. My big problem as a kid was anxiety.

Holly

Crohn's

SCD 12/01/08

>

> > No, genetic. The genetic lack of an immune system protein.

>

>

> Speaking of genetics and UC, my parents told me that when I was a

> baby, I had really bad colic, which has to do with your gut. Just

> wondering if there's any correlation, like what percentage of people

> with gut issues now had that when they were little...?

>

> Pour Dieu, pour terre,

> Alyssa =D

>

[Guest guest]

i think that if you start asking around, anxiety (being a worry wort) & stress

will be something most of us have in common.

i too was a kid that would get sick once or twice a year, especially during

winters, more so than any of my friends. later in life as a teenager, i took

erythromycin for acne. i didn't get UC until i turned 31 and it followed

immediately after a sever food poisoning on a trip to North Carolina, at a UNC

pub. i was sick like a dog for a week and so was my wife. after that i started

noticing occasional blood spotting on my stool. and it just progressed steadily

from that. i followed my regular diet for two years until a recent flare-up

that was the real thing. before that, coffee and beer seemed to be two things

that aggravated my condition the most. it is interesting how UC just

accelerates the rate of deterioration with time.

> >

> > > No, genetic. The genetic lack of an immune system protein.

> >

> >

> > Speaking of genetics and UC, my parents told me that when I was a

> > baby, I had really bad colic, which has to do with your gut. Just

> > wondering if there's any correlation, like what percentage of people

> > with gut issues now had that when they were little...?

> >

> > Pour Dieu, pour terre,

> > Alyssa =D

> >

>

[Guest guest]

This article was posted on the Yahoo PSC Support group I belong to for

my husband's autoimmune liver disease (which causes Crohns or UC, 75% of

the time).

Enzyme Involved In Inflammatory Bowel Disease Discovered At Penn State

College Of Medicine

Main Category: Crohn's

Also Included In: Irritable-Bowel Syndrome; Immune System / Vaccines;

Biology / Biochemistry

Article Date: 03 Jun 2009 - 5:00 PDT

Researchers at Penn State College of Medicine, working with biochemists,

geneticists and clinicians at the University of Bern, Switzerland and in

the United Kingdom, have discovered an enzyme that has a key role in

inflammatory bowel disease (IBD). The team, co-led by Judith Bond,

Ph.D., Distinguished Professor and Chair of Biochemistry and Molecular

Biology at Penn State College of Medicine, and Lottaz, Department

of Rheumatology and Clinical Immunology at the University of Bern,

Switzerland, could potentially lead to therapies to help the

half-a-million Americans affected by ulcerative colitis and Crohn's

disease, collectively referred to as IBD.

The enzyme, coded for by the MEP1A gene, is a zinc-containing

metalloprotease called meprin, and is abundant in the intestine. A

protease is an enzyme that breaks down proteins in the body.

Researchers at Penn State College of Medicine studied the role of meprin

in IBD using genetically altered mice lacking the ability to produce the

enzyme in collaboration with colleagues in Switzerland who studied the

enzyme in IBD patients. Meprin is abundant in the latter part of the

small intestine, or terminal ileum, and is also present in the large

intestine at a lower level. The European researchers found an alteration

in the meprin gene that correlated with IBD. They then compared the

levels of meprin in affected and unaffected sections of colons from IBD

patients and from healthy people. The amount of enzyme in the IBD

patient's inflamed colon was significantly lower than that in normal

colon sections. The researchers concluded that their findings strongly

correlate the severity of inflammation associated with both Crohn's

disease and ulcerative colitis with low meprin levels.

" This discovery is a major advance in understanding the genetic control

of inflammation, and of ulcerative colitis and Crohn's disease in

particular, " Bond said. She discovered meprin more than 25 years ago

while at the Medical College of Virginia Commonwealth University. Since

then, she has studied the structure and activities of the meprins and

has located the genes for the subunits in both the mouse and human

chromosomes. After coming to Penn State Hershey in 1992, her studies

have focused on the biomedical significance of the meprin proteases.

With colleagues from the National Institutes of Health, she found a

linkage between the meprin gene and vulnerability to diabetic

nephropathy in Pima Indians in the southwestern United States.

" These types of transitional research that provide sound basic

understanding of a disease process, coupled with detailed examination

and critical interpretation of clinical findings, are dependent upon

sustained collaborations based upon trust and respect, " Bond said.

Before this international effort, she teamed up with kidney specialists

at Albert Einstein College of Medicine in New York and with W.

Reeves, M.D., at Penn State Hershey to demonstrate that meprin

influences the outcome of acute renal failure in mice.

The Penn State researchers used a mouse model of IBD, replicating

inflammation in the intestine like that in human ulcerative colitis.

Mice lacking meprin had more severe intestinal damage after drinking a

solution to induce inflammation, than did the wild-type mice that have

meprin. These results indicate that meprin reduces the level of

inflammation in the injured intestine.

In the mouse model, it is possible to make detailed measurements on a

number of consequences of inflammation. Nitric oxide in the blood is an

important host defense against bacterial infection, but its power as an

oxidant also damages host tissue. A nitric oxide level in the blood of

mice lacking meprin was much higher than the level in wild-type mice.

The Penn State team also discovered that meprin is able to activate an

inflammatory serum factor produced by white blood cells, and this factor

is elevated in both the mouse model of IBD and in humans with active

IBD. Bond explained, " The defect in the human meprin gene most

associated with ulcerative colitis is in a region that regulates

production of the meprin protein. "

The researchers concluded that a particular defect in the MEP1A gene is

an indicator of vulnerability to IBD, particularly ulcerative colitis.

The association of the meprin gene with Crohn's disease remains to be

characterized but disruption of the meprin gene affects the severity of

both ulcerative colitis and Crohn's disease. Bond summarized the

findings by saying, " There's the possibility of predicting who will be

susceptible to IBD, and diagnosing the disease with this information. If

we could increase meprin production, or replace it with an equivalent

enzyme, there are therapeutic possibilities. More studies are needed to

understand how meprin influences inflammation, but this is the first

association of meprin levels as a key factor in the severity of IBD. "

Other Penn State College of Medicine researchers include Sanjita

Banerjee and Gail L. Matters, Ph.D., in the Department of Biochemistry

and Molecular Biology, and Leo Fitzpatrick, Ph.D., in the Department of

Pharmacology.

Source:

G. Solovey

Penn State Hershey Medical Center, Penn State College of Medicine

--

Hussey

Wife of Fred, PSC 03/04, UC 0306, SCD 04/09 (started in the hospital!!Talk about

TOUGH!