Autistic Kids and GI Problems Linked

http://ivanhoe.com/channels/p_channelstory.cfm?storyid=24218

Autistic Kids and GI Problems Linked

(Ivanhoe Newswire) -- Parents of autistic teens often report that their children suffer gastrointestinal (GI) issues like diarrhea and constipation, but new research confirms almost half of kids with an autism spectrum disorder (ASD) have such symptoms.

About one in 110 children in the U.S. has autism, a brain disorder that affects behavior, social skills and communication.

The study, conducted by the Autism Speaks' Autism Treatment Network and involving 1,185 children, also found those symptoms worsen as a child ages. At the time of enrollment, 45 percent of the children had GI symptoms. Older children reported symptoms more often than younger children: 39 percent of those under 5 years of age versus 51 percent of kids 7 years and older.

GI symptoms were also linked to sleep problems. Seventy percent of kids with GI symptoms suffered sleep problems compared to 30 percent who didn't have GI symptoms.

"These findings suggest that better evaluation of GI symptoms and subsequent treatment may have benefits for these patients," Daniel Coury, M.D., medical director of the ATN and professor of pediatrics and psychiatry at The Ohio State University, was quoted as saying. "Primary care physicians and specialists should ask families about these symptoms and address these as part of the overall management plan for the child or adolescent with ASD."

Source: Pediatric Academic Societies (PAS) annual meeting, May 1-4, 2010, Vancouver, British Columbia

Wakefield’s Lancet Paper Vindicated – [Yet Again]

http://childhealthsafety.wordpress.com/2010/05/06/wakefield’s-lancet paper vindicated/

New independent research presented at the 2010 Pediatric Academic Societies Annual Meeting in Vancouver, Canada confirms unequivocally the findings of Dr Andrew Wakefield’s 1998 Lancet paper of an association between autism and serious gastrointestinal disease in children.

The new study was conducted by the Autism Speaks Autism Treatment Network and covered data from 15 treatment and research centers in the United States and Canada. Of 1185 children aged 2 to18 years with an autistic condition 45% were reported to have GI symptoms. Abdominal pain was most common (59%) followed by constipation (51%), diarrhea (43%), other (40%), nausea (31%) and bloating (26%). Reports of GI symptoms increased with age. Sleep problems occurred in 70% of children with than those without GI symptoms (30%). The problems affected all children regardless of gender, ethnic background or intelligence.

This is not the first time Wakefield’s research has been confirmed by independent researchers around the world. Read a previous article and see the list of papers replicating Wakefield’s Lancet paper research: Sunday Times’ Discredited – Wakefield’s Autism Research Verified

Additionally, one of the witnesses in the GMC proceedings against Dr Wakefield writing to the British Medical Journal confirmed the validity of the histopathology on which the paper was based and illustrated how Sunday Times journalist Brian Deer had misrepresented her evidence. Dr Susan E Davies, Consultant Histopathologist, Addenbrooke’s Hospital, Cambridge stated in the British Medical Journal regarding a BMJ article by Brian Deer that “There is some misrepresentation …. and lack of understanding of the process in studies involving histopathology.” and that there were significant findings “While a clinical gastroenterologist might consider caecal active inflammation with incipient crypt abscess formation to be normal in children (1), this is a significant finding to be recorded by pathologists“: “Caution in assessing histopathological opinions.” BMJ Rapid Responses 30 April 2010.

So will Dr Richard Horton, editor of The Lancet now “unretract” The Lancet paper?

Thanks. The connection between GI problems and autism/CFS seems to be very strong.

I thought I would post that I just received my ASD son's stool results yesterday. According the results, the concentration of sigA (secretory IgA) is abnormally high. The yeast cultered from the stool specimen is considered dysbiotic. There were some other irregularities as well. What gets me is that it is so well known that ASD people have these problems and yet my kid's pediatrician never ordered this test. I had to go to a biomed doctor and pay for these tests out of pocket. Anyway, I see the doctor again at the end of this month and look forward to hearing all the other test results.

Good luck, Jill. Stick to your guns about this. My son's mental health recovered as a result of sorting his guts out.

i'm pretty sure you can link those gut problems further, with all kinds of allergies and sensitivities.

New autism study in Houston

http://abclocal.go.com/ktrk/story?section=news/health&id=7353260

HOUSTON (KTRK) -- Doctors have suspected a link between autism and digestive problems for years. Now Houston researchers are testing a drug with such potential, that the Food and Drug Administration has fast-tracked it. Scientists believe it may improve autistic behaviors.

Doctors believe many children with autism can't digest protein, which would cause them to lack amino acids that are critical in producing neurotransmitters for the brain. They believe resolving the digestion problem may help the autism.

Very interesting, maybe this has implications for CFS. Does anyone know what medication they use?

Very good question. I asked a parent if this was Cytoflora and she said yes but I would like to get this validated by another source. Does anyone else here know? I would really like to try this on my son.

I am so glad people are taking this issue seriously. There is no doubt that certain foods have a profound effect on my sons behavior. I am very interested in this drug and am going to look into this.

Does anyone know of a good overview type article from a reputable source on GI issues (and possible treatments) for kids in the autism spectrum?

Hi ...I hope this information helps and answers some of your questions....

The autism study mentioned refers to the use of a medication/drug, however the product used sounds like an enzyme based product [digestive enzyme] which will break down and digest protein...

the product used is actually called CM-AT.

Quote from recent research..

" CM-AT is based on breakthrough research that showed enzyme deficiencies in autistic children, resulting in an inability to digest protein. The inability to digest protein affects the production of amino acids, the building blocks of chemicals essential for brain function. CM-AT will be one of the first therapies to address the underlying physiology of autism, rather than just treat its symptoms."

The company organising the Curemark CM-AT autism trials is called CUREMARK LLC

Further information About CUREMARK LLC

Curemark is a drug research and development company focused on the treatment of neurological and other diseases, especially those with dysautonomic components, by addressing certain key gastrointestinal/pancreatic secretory deficiencies. The company's initial products are based upon breakthrough observations by its founder, Dr. Joan Fallon, which revealed a lack of protein digestion in children with autism and ADHD. To learn more about our innovative science, visit

http://www.curemark.com/

Curemark is Enrolling Patients In Phase III Autism Trials At Ten Sites

Source: Curemark, LLC .... Please note this information dates back to January 25, 2010

RYE, N.Y., Jan. 25 /PRNewswire/ -- Curemark, LLC, (www.curemark.com), a drug research and development company focused on the treatment of neurological diseases, announced that the company is now enrolling patients in Phase III clinical trials for CM-AT, its autism treatment, at ten sites across the country. The sites are:

Curemark's Phase III trials for CM-AT encompass 12 sites nationally with a total 170 children.


"We have six new trial sites that are now active and recruiting patients - New York, Philadelphia, Houston, Indianapolis, Columbus and Shreveport. These are in addition to the four that we announced had opened enrollment in October and November," said Dr. Joan Fallon, Curemark founder and CEO. "We're moving very rapidly with our clinical trial program and anticipate that the remaining sites will be initiating enrollment soon."


CM-AT is based on breakthrough research that showed enzyme deficiencies in autistic children, resulting in an inability to digest protein. The inability to digest protein affects the production of amino acids, the building blocks of chemicals essential for brain function. CM-AT will be one of the first therapies to address the underlying physiology of autism, rather than just treat its symptoms.


"We're hopeful about the viability of Curemark's enzyme replacement therapy and the promise of CM-AT in targeting the physiology of autism for the first time," Fallon said.


New data released in December by the U.S. Centers for Disease Control and Prevention (CDC) indicated that the number of children affected by autism is higher than originally thought. According to the CDC, autism affects 1 in 110 children.


For information on participating in the Curemark CM-AT autism trials, log on to www.clinicaltrials.gov and search "Curemark."

Further information ...

CM-AT, an orally ingested powder that delivers protein-digesting protease,

CM-AT is a proprietary enzyme that is designed as a powder taken three times a day.

http://www.clinicaltrials.gov/ct2/show/NCT00881452?term=curemark&rank=1

I emailed a friend today about this study. She said she had looked into this study for her son but they never returned her email She found that this is a pancreatic enzyme that would, likely, not work any better than the enzyme (TriEnza) which we both currently give our children. Her concern was having to take her son off all his other supplements and treatments and did not think it was worth it.

Jewel, there are 3 very good studies that came out recently, 2 are actually reviews and consensus recommendations by top guns pead gastros in the US (mainstream, believe it or not), published in January issue of Pediatrics.

3rd is a large scale study by Autism Treatment Network ATN.

They are all linked on this site, let me know if any problems http://www.treatingautism.co.uk/

As for the actual 'treatments' in the real world, there are many people try, what works and what not mainly down to individuals. Most success overall with digestive enzymes, probiotics, cultured foods, SCD diet, GFCF diet, staying Igg allergen free... many herbals are used as well in general

Funnily enough several people report dramatic overnight improvements in GI symptoms once they start rx antivirals, like valtrex.

Thank you very much!

Also very worthwhile looking at Dr Krigsman's research
Dr. Krigsman is an expert in G.I pathology in Autism, he specialises in treating children with Autism Spectrum Disorders and he has performed endoscopies on 100's of children & he has found lesions in their gastro-intestinal tracts.
Dr Krigsman states that these lesions are treatable through a combination of restricted diet, anti-inflammatories, probiotics, anti-fungals & digestive enzymes.

G.I Pathology In Autismescription & Treatment

http://www.medicalveritas.com/AKrigsman.pdf

Dipeptidyl peptidase IV or DDP-IV, appears to be absent or reduced in autistic children.

http://www.healing-arts.org/children/autism-overview.htm#Dipeptidyl Peptidase Deficiency

Dipeptydal peptidase deficiency:

Alan Friedman and colleagues have pioneered the potential role of DPP IV deficiency in autism. Some have gone so far as to suggest that DPP-IV deficiency may explain all of the abnormalities seen in autism. Dipeptidyl peptidase IV (DPP-IV) is a serine peptidase that removes N-terminal dipeptides sequentially from polypeptides having unsubstituted N-termini provided the penultimate residue is proline.

The only known enzyme to break down casomorphine, dipeptidyl peptidase IV or DDP-IV, appears to be absent or reduced in autistic children. The gene for this enzyme is distal to other suspected autism genes on 2 and Q of 7 and is expressed in the kidney, the small intestine, the liver, the blood-brain barrier, and has involvement in T-Cell activation. Also found in the urine were undigested food particles, suggesting a leaky gut syndrome.

Mice with the a defective casomorphine enzyme gene will die if not on a gluten free diet. Later we will discuss the possible role of glutein and cassein in autism, and the elimination of these substances from the diet as a treatment. The toxicity of gluten and cassein may result from the lack of DPP IV. Thus, DPP deficiency may be important in explaining opioid excess.

DPP IV has a number of different names. When it is present on the surface of a T-cell it is called CD26.

Dr. Friedman postulates that DPP-IV is either absent via a genetic mechanism (probably through two recessive genes) or that the enzyme has been inactivated, possibly through autoimmune mechanisms (a theory of autism which we will cover later). It has been postulated that people, autistic from birth, produce no DPP-IV, and those who developed normally and then regressed, had their DPP-IV inactivated through an acquired mechanism (such as auto-immunity) .

One such compound is dermorphin, a mu-opioid agonist that acts as an hallucinogen. Another is deltorphin II. Some researchers theorize that these compounds appear because the enzyme which cleaves certain peptide bonds (DPP IV) is either missing or inactivated. Gluten and casein are two of the proteins from which these opioids can be produced. There may be additional proteins for which this is true as well.

" If DPP IV deficiency results in autism, what can be done? If the enzyme is missing, replacing it should solve the deficiency "

Theories of Potential Therapies for DPP IV Deficiency [Unevaluated]:

If DPP IV deficiency results in autism, what can be done? If the enzyme is missing, replacing it should solve the deficiency. DPP IV is found on intestinal mucosal cells, epithelial cells in the GU tract, and on the surface of T-cells. It might be possible to hook the DNA sequence coding for DPP IV onto some type of delivery mechanism (such as a plasmid) and infuse the plasmids into the patient so that the desired sequence would be incorporated into the patient's DNA. Another alternative is stem cell therapy or live cell therapy. Injected cells might produce DPP IV which would migrate to areas in which it is needed.

If the enzyme is inactivated by an autoimmune mechanism, replaced enzyme would probably be inactivated as well.

Here is a the skeleton for a future treatment: Drucker, et al. 2 studied DPP-IV deficicient rats. Administration of GLP-2 to these rats was associated with a markedly increased bioactivity of rat GLP-2 resulting in a significant increase in small bowel weight. A synthetic GLP-2 analog, r[Gly2]GLP-2, with an alanine to glycine substitution at position 2, was resistant to cleavage by both DPP-IV and rat serum in vitro. Treatment of wild-type rats with r[Gly2]GLP-2 produced a statistically significant increase in small bowel mass. DPP-IV-mediated inactivation of GLP-2 is a critical determinant of the growth factor-like properties of GLP-2. The possibility exists that treatment of autistic people with sufficient quantities of GLP-2 or with synthetic r[Gly2]GLP-2 which cannot be cleaved by DPP-IV would alleviate symptoms associated with autism.

Drucker DJ, DeForest L, and Brubaker PL have shown that GLP-2-like compounds have potential use for enhancement of mucosal regeneration in patients with intestinal disease 3. This may relate to autistic children who have gastrointestinal symptoms. Findings such as these may explain the usefulness of hormonal therapies for autistic children's gut problems.

GLP-2 is part of proglucagon, which also contains GLP-1. Proglucagon is secreted from enteroendocrine cells of the small and large intestine. GLP-1 lowers blood glucose in both NIDDM and IDDM patients and may be therapeutically useful for treatment of patients with diabetes. GLP-1 regulates blood glucose via stimulation of glucose-dependent insulin secretion, inhibition of gastric emptying, and inhibition of glucagon secretion. GLP-1 may also regulate glycogen synthesis in adipose tissue and muscle; however, the mechanism for these peripheral effects remains unclear. GLP-1 is produced in the brain, and intracerebroventricular GLP-1 in rodents is a potent inhibitor of food and water intake. The short duration of action of GLP-1 is accounted for in part by dipeptidyl peptidase 4 (DPP-IV), which cleaves GLP-1 at the NH2-terminus; hence GLP-1 analogs or the lizard peptide exendin-4 that are resistant to DPP-IV cleavage are more potent GLP-1 molecules in vivo. GLP-2 has recently been shown to display intestinal growth factor activity in rodents, raising the possibility that GLP-2 may be therapeutically useful for enhancement of mucosal regeneration in patients with intestinal disease.