celiac / enzyme, was, ...about your blurb, was, more about cod liver

[Guest guest]

I did a quick search. Found a couple related abstracts. Haven't really

looked at them yet, but for those interested in this tangent, have

them pasted below. wishing all the best answers, elizabeth

******

http://www.ncbi.nlm.nih.gov/pubmed/16793522

1: Chem Biol. 2006 Jun;13(6):649-58.

Rational design of combination enzyme therapy for celiac sprue.

Siegel M, Bethune MT, Gass J, Ehren J, Xia J, Johannsen A, Stuge TB,

Gray GM, Lee PP, Khosa C.

Department of Chemical Engineering, Stanford University, Stanford,

California 94305, USA.

Celiac sprue (also known as celiac disease) is an inheritable,

gluten-induced enteropathy of the upper small intestine with an

estimated prevalence of 0.5%-1% in most parts of the world. The

ubiquitous nature of food gluten, coupled with inadequate labeling

regulations in most countries, constantly poses a threat of disease

exacerbation and relapse for patients. Here, we demonstrate that a

two-enzyme cocktail comprised of a glutamine-specific cysteine

protease (EP-B2) that functions under gastric conditions and a PEP,

which acts in concert with pancreatic proteases under duodenal

conditions, is a particularly potent candidate for celiac sprue

therapy. At a gluten:EP-B2:PEP weight ratio of 75:3:1, grocery store

gluten is fully detoxified within 10 min of simulated duodenal

conditions, as judged by chromatographic analysis, biopsy-derived T

cell proliferation assays, and a commercial antigluten antibody test.

PMID: 16793522 [PubMed - indexed for MEDLINE

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http://www.ncbi.nlm.nih.gov/pubmed/18425213

1: PLoS Pathog. 2008 Feb;4(2):e34.

Parallels between pathogens and gluten peptides in celiac sprue.

Bethune MT, Khosla C.

Department of Biochemistry at Stanford University, Stanford,

California, United States of America.

Pathogens are exogenous agents capable of causing disease in

susceptible organisms. In celiac sprue, a disease triggered by

partially hydrolyzed gluten peptides in the small intestine, the

offending immunotoxins cannot replicate, but otherwise have many

hallmarks of classical pathogens. First, dietary gluten and its

peptide metabolites are ubiquitous components of the modern diet, yet

only a small, genetically susceptible fraction of the human population

contracts celiac sprue. Second, immunotoxic gluten peptides have

certain unusual structural features that allow them to survive the

harsh proteolytic conditions of the gastrointestinal tract and thereby

interact extensively with the mucosal lining of the small intestine.

Third, they invade across epithelial barriers intact to access the

underlying gut-associated lymphoid tissue. Fourth, they possess

recognition sequences for selective modification by an endogenous

enzyme, transglutaminase 2, allowing for in situ activation to a more

immunotoxic form via host subversion. Fifth, they precipitate a T

cell-mediated immune reaction comprising both innate and adaptive

responses that causes chronic inflammation of the small intestine.

Sixth, complete elimination of immunotoxic gluten peptides from the

celiac diet results in remission, whereas reintroduction of gluten in

the diet causes relapse. Therefore, in analogy with antibiotics,

orally administered proteases that reduce the host's exposure to the

immunotoxin by accelerating gluten peptide destruction have

considerable therapeutic potential. Last but not least,

notwithstanding the power of in vitro methods to reconstitute the

essence of the immune response to gluten in a celiac patient, animal

models for the disease, while elusive, are likely to yield

fundamentally new systems-level insights.

PMID: 18425213 [PubMed - indexed for MEDLINE]

PMCID: PMC2323203

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http://www.ncbi.nlm.nih.gov/pubmed/17438672

1: Ann Med. 2006;38(8):578-91.

Understanding the molecular basis of celiac disease: what genetic

studies reveal.

Monsuur AJ, Wijmenga C.

Complex Genetics Section, Department of Biomedical Genetics, UMC

Utrecht, The Netherlands.

Celiac disease (CD) is characterized by a chronic immune reaction in

the small intestine to the gluten proteins that are present in a

(Western) daily diet. Besides the well known involvement of the HLA

class II histocompatibility antigen (HLA)-DQ2.5 and -DQ8 heterodimers

(encoded by particular combinations of the HLA-DQA1 and -DQB1 gene) in

CD and the minor contribution of the CTLA-4 gene, recently the myosin

IXB (MYO9B) gene has also been found to be genetically associated.

This review covers the general aspects of CD as well as current

insight into important molecular aspects. We evaluate the role of

susceptibility genes in CD by following gluten along its path from

ingestion to uptake in the body, which leads us through the three

aspects of CD's pathology. The first is the presence of gluten in the

lumen of the intestine, where it is broken down by several enzymes.

The second is the intestinal barrier through which gluten peptides

pass. The third is the reaction of the immune system in response to

gluten peptides, in which both the innate and the adaptive immune

systems play a role. Our main conclusion, based on the current genetic

and functional studies, is that we should look for causal genes in the

barrier function as well as in the immune systems.

PMID: 17438672 [PubMed - indexed for MEDLINE]

> >

> >

> > ----- Original Message -----

> > From: eli8591

> >

> >

> >

> > Do have any related tidbits such as this - this particular Irish

> > tendency is not one that I have come across, and helps explain our

> > problems with flax a tad more...aannnddd, do you have references for

> > this??? I would really like to look into this more...is it tied into

> > the celiac/irish connections? chuckling, etc,etc,etc....

> >

> > ===>Andy was my source, told me this, and I don't know if there

is a connection

> between this and celiac. We are not celiac, she has always eaten

whole wheat without

> problem, but could be a connection somewhere. You might ask Andy

about his source.

>

> It seem,s to be generally accepted amongst nutritionlists I believe

are sanea nd

> knowledgeable (a small subset unfortunateyl) that some people of

Irsih descent lack one

> of the enzymes tht turns the alpha linolenic acid in flax oil intoo

the EPA and DHA thta

> people actually need. Fish oil contains EPA and DHA< no conversion

needed.

> >

> >

> >

> > thanks for any ideas/comments, wishing you the best, elizabeth

> >

> > (snipped)

> > > There are flax oil and hemp oil. Excellent products.

> > >

> > > ==>We can't do flax, Irish here and many Irish do not convert

> > flax, fish oil works just fine.

> > >

> > >

> >

> >

> >

> >

> >

> >