100 people - 1 with celiac disease

Of these, in Australia only 25% know they have celiac disease.
Until recently, the figure in North America was 5%
That's half a million people probably, unaware they have it!


Weigh your babies regularly, record on a percentile chart...

coeliac disease infant weight charts

These are two infant weight charts, showing failure to thrive because of coeliac disease.

The black lines are expected growth for the 90th and 10th percentiles - 90% and 10% at or below that weight for age.

These infants initially grew parallel to the percentile lines, at their expected rates. Growth then slowed, after 6 (red) and 4 (blue) months, with introduction of cereal.

age distribution celiac diagnosis


Better to know now, not years later.



The peaks of the age at diagnosis were infancy and 40 years old, with people being first diagnosed up to age 80!


This is a lifelong susceptibility to bowel damage by our immune system, when exposed to gliadin peptide in cereals. The small bowel loses its microscopic finger-like projections and becomes flat.

As well as this severe reduction in surface area, the lining cells now don't last long enough to develop fully, before they are shed and replaced.

The enterocytes therefor never get to express all their digestive enzymes, such as lactase.

The net result is reduced ability to digest and absorb our food.

The damage to the bowel wall increases the permeability to large molocules, including gliadin, so it becomes a viscious circle - more damage, more damaging gliadin absorbed.


Prevention of celiac disease

Infancy

Gradual introduction of gluten containing cereal at about 4-6 months (not in the first 3 months,) was believed best, rather than holding off until about 1 year old, which was thought to be counter productive. This has now been turned on its head with the publication of a prospective double blind randomized controlled trial.⁵

Later

Tissue transglutaminase (tTG) is an extracellular enzyme in between the cells, in the connective tissue of our small bowel wall. It is here within the wall of our small bowel, that it acts on the digestion resistant peptides (fragments of proteins - here gliadin.)

This starts the disease process which damages the bowel.

Preventing the gliadin from getting into the bowel wall in the first place, should be a priority.

Secretory antibodies of the IgA class (sIgA) are thought to have an important role in the defense against bacteria at mucosal surfaces, where the infectious agents first come into contact with the host.

These secretory antibodies can bind multiple antigens. They have "skeleton key" specificities. They are thought also to eliminate self-antigens to avoid systemic recognition. This protects us from auto-immune diseases.

They also function to prevent partly digested food from getting into the bowel wall - the critical thing here.

Bovine colostrum produced a 79% increase in sIgA over 12 weeks, in a trial in athletes by Crooks et al published in 2006.

Medical research on prevention is not being directed towards producing oral tolerance, because the bowel is the target organ and is extremely sensitive to start with.

There must be lots of other ways to increase this first line of defense by the layer of sIgA coating the inside of our bowel.

Ensuring adequate good quality protein and zinc in our diet, would be starters.

Avoiding drugs which cause bowel damage and practicing good food combining (see below), could also be useful.



Infancy and beyond, celiac disease in childhood and adolescence.

These should alert one to the possibility of coeliac disease....

Infancy to preschool..

Failure to thrive or weight loss.
Chronic diarrhoea or occasionally constipation.
Irritability or lethargy
Big tummy

Five years and beyond..

Unexplained recurrent abdominal pain
Iron deficiency anaemia
"A bit cranky and not themselves."
learning difficulty
Delayed puberty may result.
Hair loss,thyroid problems, chronic headaches, early osteoporosis, elevated liver enzymes or leg pains, may give a clue to this.

Rheumatologists at the NY Hospital For Special Surgery⁶ found their children had at least double the chance of also having coeliac disease. Two thirds of those newly discovered by their screening tests, had no tummy troubles at all.


Adult celiac symptoms

Fatigue
Flatulence and bloating
Deficiency of iron, folic acid, zinc
Recurrent mouth ulcers
Infertility or recurrent miscarriages
Osteoporosis and multiple fractures - very common
Dermatitis herpetiformis, an itchy skin rash
Epilepsy, ataxia, unexplained neurological problems
Septicaemia, meningitis, pneumonia
Irritable bowel syndrome plus iron deficiency
Thyroid problems

Everyone with irritable bowel syndrome is strongly advised to get a screening test for coeliac disease. A test of serum calcium level and an upper abdominal ultrasound are also good ideas.

Men with celiac disease can have hypogonadism, immature secondary sex characteristics and reduced semen quality.
Hyperprolactinaemia causes impotence and loss of libido in some.

Family history

An identical twin with celiac gives you a 70% chance of getting it too, so heredity is important.

If you have a first degree relative with celiac, a negative serology test is not good enough.

The problem is that so few people with celiac disease have been diagnosed. If you can recognize symptoms above in a first degree relative, perhaps you should both get checked.

People can have positive antibody tests and villous atrophy on biopsy, but with few or no symptoms. These include many family members of coeliac patients.

The have "silent coeliac disease."
People with positive antibody tests but normal small bowel mucosa, are referred to as having "latent coeliac disease."


Celiac disease diagnosis - how to check

New blood tests are being continually developed, such as Anti-reticulin antibody (ARA) and now deamidated Gliadin Peptide (DGP) assays.

The anti tissue transglutaminase (tTG) blood test is not as accurate as formerly believed. Only 50% of people with this +ve, have celiac disease on biopsy, so it is really only a screening test.

It picks up 80% of celiac disease, provided that the people have been eating gluten at the time (eg. 4 slices of bread a day.)

A total IgA test is needed with any IgA antibody test, as some people are deficient in this class of antibodies - making the test inaccurate. These people are also actually at an increased risk of having celiac, to boot.

If someone has already been on a gluten free diet, the gene test (HLADQ2) can be used. One study showed that of every twenty people on a gluten free diet, only one of them had celiac disease. A negative gene test will tell if you are one of the other 19.

You can be allergic to wheat and the other cereal grains without having celiac disease.

The gene test is not much use for diagnosing celiac though, as it is positive in about a third of the healthy population. It is only useful for ruling out the diagnosis.

It is more use in children, people already on a gluten free diet and people with +ve antibody tests but negative small intestinal biopsy.

Small bowel biopsy at the start, when eating a regular diet including enough wheat, on a gluten free diet and finally later following a gluten challenge - 3 in all, wraps it up nicely.

A gluten challenge test should not be undertaken for at least two years and preferably not before 6 years age because it can otherwise damage the dentition. It is usually delayed until catch–up growth has been completed.

The gluten challenge is needed for several months, before the repeat biopsy.

This possibly sounds a bit over the top, but it is a lifelong disease with an increased risk of lymphoma if untreated, so accurate diagnosis is pretty important.



Abdominal ultrasound signs include...

Increased fasting gallbladder volume
The presence of free fluid in the peritoneal cavity around the bowel
Enlarged lymph nodes in the mesentery which suspends the bowel.
Increased peristalsis - movement of the bowel
Intestinal dilatation - increased transverse diameter of small bowel.
Thickness of the small bowel wall.

An Italian study¹ claimed this to be an effective way of confirming the diagnosis. These findings may raise the question of celiac disease.





Transaminitis - a tongue in cheek term for unexplained elevation of liver enzymes alanine transaminase (ALT) and  aspartate transaminase (AST) is another finding that should alert one to the possibility of celiac disease.

Non-Celiac Gluten Sensitivity

Non celiac gluten intolerance is around 30 times more prevalent than coeliac disease. Up to maybe 30% of people are gluten sensitive.

These are people who don't have proof, even though they feel better off gluten.

You can read Dr. Scot Lewey on this subject, at

www.celiac.com. He is a gastroenterologist with this condition, and broad minded.

A neurologist Dr. Perlmutter also talks a lot about this³, to quote

"When I finally began to understand what the proximate cause of the various illnesses we were dealing with was, I realized that mainstream neurology, though I don’t want to sound too critical, really pays no attention to the causation part of the story."

Do you feel better on a gluten free diet? You may have only wheat intolerance and not need to have only the foods on a gluten free foods list. It's worth trying to find out what applies to you.

You really need to know the attitude of the gastroenterologist, because lots will obviously not consider NCGS.

Further reading on gluten is available on greenmedinfo.com if you agree to get his daily e-mails, which are very good value quite apart from this offer.

Diet management of coeliac disease

It is very difficult, and so get all the help you can. There is wheat in just about everything at the supermarket (well nearly.)

Even tiny amounts of gluten are harmful.

About half of all people with diagnosed coeliac disease, are not in remission.

A repeat biopsy when apparently on a correct diet, is very useful for checking (and for giving a prognosis.) Incomplete healing is not a good sign.

An annual checkup is worthwhile, especially with a dietician skilled in coeliac disease. Lifelong total avoidance of gluten is needed and one needs to keep up with developments in best care. Blood relative should be tested.

From celiac disease back to home page


A full script article on oats is at...

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1774046

They were to do a 5 year follow up, which I've yet to find.



This is about a 16 year old teenager whom I saw 40 years ago.

He came in complaining of easy bruising for one month and spontaneous bruising and bleeding gums for two days.

He had a past history of iron deficiency anaemia, and for as long as he could remember had pale, bad smelling half liquid faeces.

He was short and lean.

His prothrombin test came back grossly prolongued, indicating lack of vitamin K, to which he responded rapidly.
X-rays showed thinning of his bones, and his calcium level was down
His red blood cells were abnormally large and his vitamin B12 low.
His duodenal mucosa was flat, with villous atrophy on biopsy.

One month later, gluten free, he was feeling well, had put on 3kgm and had grown 2.5cm.



Further notes on tissue transglutaminase (tTG or TG2)

This tTG enzyme, like xanthine oxidase, is involved in cleaning up operations in our body - here "deamidation" (conversion of glutamines in the gliadin to glutamic acid.)

This change leads to better binding of the peptides to HLA and more efficient recognition by gliadin specific T cells (so faster clearance of the foreign material.)

Another of the functions of tTG is to form the "apoptotic envelope" which prevents escape of intra-cellular contents during programmed cell death.

It has been suggested that lack of tTG may encourage autoimmunity.

I wonder whether using up one's tTG while dealing with gliadin, may result in a consumptive deficiency and hence the autoimmune damage seen in celiac disease.

tTG is induced (increased) by proprionate and butyrate - short chain fatty acids from good germs in our bowel eating fiber. I wonder if a good diet with plenty of soluble vegetable fiber, may be protective against celiac.


ps Apparently gluten peptides can also be modified by tTG by transamination, with cross-linking of a glutamine in the gliadin peptide to a lysine in the tTG itself.

This change in the tTG renders it "foreign" and antibodies against it are produced. This would also reduce tissue concentration of tTG.


If you are an immunologist reading this, I would appreciate your contact with feedback.

Glyphosate may be the ultimate dark horse.

Stephanie Seneff⁴ noted the close parallel between the increasing use of glyphosate and the incidence of coeliac disease. Her papers with Anthony Samsel are about the connection,

celiac disease and adenovirus 12

This association is particularly interesting.
One of the virus proteins, Elb protein, has a similar amino acid sequence to that in gluten peptides.

Infection with adenovirus and subsequent exposure to gliadin could trigger the development of CD, from immune cross reactions.

Food combining

This refers to the variety of foods one includes in a meal, to be eaten at the same time.

One proposition is that eating a lot of carbohydrate at the same time as protein, makes it harder for the stomach to get the pH down adequately.

The same applies to drinking a lot of liquid with a protein meal.

It is a dilution effect - a bigger volume of gastric contents requires more acid to achieve the concentration needed.

There are a lot of rules, such as fruit on its own, melon on its own, carbs and fats ok together etc. I don't understand any other underlying principles nor explanations, and would be very happy for feedback on this.

The intention is to facilitate digestion - to make it easy on one's GI system.

Nutritional and herbal support.

Probiotics, L-glutamine, L-carnitine, zinc and copper may be useful, as well as the expected things such as iron, B 12, vitamins K etc.

Botanicals such as deglycyrrhizinated licorice, marshmellow root, lemon balm and chamomile may also be useful.

References and notes for celiac disease page

1. Fraquelli et al Archives of internal medicine. 2004; 164(2):pp169-74.

2. HLA-DQ2 and occasionally HLA-DQ8 are present in nearly all people with coeliac disease. These molecules pass the deamidated gliadin on to T helper lymphocytes.


3. http://articles.mercola.com/sites/articles/archive/2013/09/29/dr-perlmutter-gluten.

4. https://groups.csail.mit.edu/sls/publications/2013/Seneff_Entropy-15-01416.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945755/

5 The 2014 study concluded...

"Early dietary factors, particularly the child's age at the introduction of gluten, seem to play a minor role in the risk of the development of celiac disease,"

http://www.nejm.org

This has been confirmed in another study published in 2015... http://pediatrics.aappublications.org/content/early/2015/01/13/peds.2014-1787.abstract

6. http://pediatrics.aappublications.org/content/early/2015/06/09/peds.2014-2379.abstract



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HLA stands for human leukocyte antigen because it was first discovered in white blood cells - leukocytes. It's also called the major histocompatibility complex (MHC) because of it's importance in tissue rejection, as after grafting kidneys or livers from donors.

It consists of molecules on the surface of special cells which bind bits of proteins from germs or cancer cells and tell the immune T cells to go fight them.






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