UCLBS News

August 6, 2005

Death of Elaine Gottschall

Filed under: News — luisa @ 10:31 pm

It is with great sadness that we announce the death of Elaine Gottschall. She passed away peacefully on Sunday, September 5th at 3:30 p.m with her daughters by her side.

Elaine has been the driving force behind SCD, dedicating her life to improving the health of those suffering from inflamatory bowel diseases. Her caring nature and devotion will never be forgotten.

October 1, 2004

Study On SCD and Autism Released

Filed under: News — luisa @ 8:04 pm

We’d like to announce the immediate release of the overviewof the study, “Specific Carbohydrate Dietary Trial:Understanding the Effectiveness of a Specific CarbohydrateDietary Intervention In Autistic Children.”
A pdf of this article is available at http://www.dream-big.us/.
Jeff and Brian

——————

Jeffrey A. Trelka
Brian S. Hooker, Ph.D., P.E.

Specific Carbohydrate Dietary Trial: Understanding theEffectiveness of a Specific Carbohydrate

DietaryIntervention In Autistic Children
Jeffrey Allen Trelka1, Brian S. Hooker2
1901 Celery Ave., Algona, WA. 98001
2503 South Young Place, Kennewick, WA 99336

Running Title: SCD & AUTISM

Corresponding Author:
Jeffrey Allen Trelka901 Celery Ave., Algona, WA.98001
Phone: (253) 833-3617
FAX: (253) 833-3617

ABSTRACT

Background: There is strong evidence supporting theories which purport that genetic connections may increase risks for autism, but the etiopathology of autism has remained undefined. In recent years, studies have focused on a diet-autism axis in an attempt to better understand nutritional contexts of autistic behavior and learning. Studies have shown that some autistic expressions may be ameliorated with a gluten free/casein free diet. A Specific CarbohydrateDietary intervention has become increasingly popular among parents of autistic children, while medical physicians have become increasingly concerned for these children’s nutritional health. Specific Carbohydrate Dietary interventions have not been scientifically evaluated.

Objective: Based on claims that the Specific CarbohydrateDiet ameliorates autistic behaviors and heals chronic gutissues, the purpose of this project is to understand theSpecific Carbohydrate Diet’s effectiveness in ameliorating autistic expressions, i.e., both behavioral andphysiological.

Design: Physiological and behavioral signs were observed in 2 children with autism. Based on the abnormal physiological and behavioral profiles, targeted dietary intervention trials using a Gluten Free/Casein Free Diet followed with a Specific Carbohydrate Diet were initiated in both autistic children.

Results: These autistic children showed significantly less behavioral and physiological problems during the SpecificCarbohydrate Diet than during the Gluten Free/Casein Free intervention. These results are consistent with the claims related to a Specific Carbohydrate Dietary intervention.

Conclusions: Based on the results of observed behavioral and physiological changes during the adherence of a SpecificCarbohydrate Dietary intervention, we hypothesize that theSpecific Carbohydrate Diet does ameliorate autistic expressions in some autistic populations.

Key Words: autistic disorder, autism, nutritionalintervention, SCD, Specific Carbohydrate Diet, GF/CF, GlutenFree/Casein Free

Acknowledgements: Statement of Author Contributions:1. Jeffrey Allen Trelka: Study design, study coordinator,data collection, interpretation of data, manuscript writing2. Brian S. Hooker, Ph.D., P.E.: critical review,interpretation of data, manuscript writing

None of the authors have any financial conflict of interest to report.

Comparison of changes observed between each intervention.
Gluten Free/Casein Free Student A GlutenFree/Casein Free Student B Specific Carbohydrate DietStudent A Specific Carbohydrate Diet Student B
Improved Behavioral Changes
    Less Stimming
    Began to speak for the first time since regression
    More vocabulary (echo)
    Improved eye contact
Loss of Self-mutilating behavior
Loss of Constant stimulating behaviors
No dietary self-limiting
No fetal positioning
No night waking
Loss of autistic gaze
Less tantrums
More words & clearer speech
More aware of environment
Greater imitation skills
Greater self-control / less hyperactive
Loss of head-banging
Less screaming & crying
More social
More helpful
Greater imagination
No dietary self-limiting
No fetal positioning
No eye covering
Significantly less night waking
Loss of autistic gaze
Less tantrums
More aware of environment
Not biting others
Less screaming & crying
More initiating
More verbalizing
Smiles & laughs appropriately
Improved Physiological Changes Diarrhea decreasedfrom approx. 7 per day to only 1 per day Diarrhea decreased from approx. 7 per day to only 1per day No food induced eczema
Solid Stool
Less abdominal distention
No Panda eyes
Loss of foul body odor
No food induced eczema
Solid Stool
Less abdominal distention
No Panda eyes
Loss of foul body odor
Deteriorating Behavioral changes Self-limiting diet Self-limiting diet
Deteriorating Physiological Changes

References
Adams, L., & Conn, S. (1997). Nutrition and Its Relationship to Autism. Focus on Autism and Other Developmental Disabilities, 12, 53-58.

Autism Research Institute. (2003-2004). Autism Treatment Evaluation Checklist (ATEC) Internet Scoring Program. Referred at: http://autism.com/atec/

Bricker, D. (Ed.). (2002). Assessment, Evaluation, and Programming System for Infants and Children (AEPS) (2nded.). Paul H. Brookes Publishing Co., Inc.

Eikeseth, S., Smith, T., Jahr, E., & Eldevik, S. (2002).Intensive Behavioral Treatment at School for 4 -7 Year Old Children with Autism. Behavior Modification, 26(1): 49-68.

Jacobson, M., & Schardt, D. (1999). Diet, ADHD and Behavior: A Quarter – Century Review. Washington, D.C.:Center for Science in the Public Interest.

Gottschall, E. (2002). Breaking the Vicious Cycle:Intestinal Health Through Diet. Baltimore, Ontario:Kirkton Press Ltd.

Horvath, K., Papadimitriou, J.C., Rabsztyn, A., Drachenberg,C., Tildon, J.T. (1999). Gastrointestinal abnormalities in children with autistic disorder. TheJournal of Pediatrics, 135(5), 559-63.

Koegel, R., Schreffirnan, L., Good, A., Cerniglia, L.,Murphy, C., Koegel, L. (2003). How to Teach Pivotal Behaviors to Children with Autism: A Training Manual.Retrieved August 1, 2003, from the University ofCalifornia, Santa Barbara: http://www.users.qwest.net/%7Etbharris/prt.htm

Knivbserg, A., Reichelt, K., Nodland, M., & Hoien, T.(1995). Autistic Syndromes and Diet: a Four Year Follow-Up Study. Scandinavian Journal of Educational Research,39, 223-236.

Knivbserg, A., Reichelt, K., Hoien, T., & Nodland, M.(2003). Effect of a Dietary Intervention on Autistic Behavior. Focus On Autism and Other Developmental Disabilities, 18(4), 247-256.

Pangborn, J., & Baker, S. (2002). Biomedical Assessment Options for Children With Autism and Related Problems:A Consensus Report of the Defeat Autism Now!S cientific Effort. Autism Research Institute. SanDiego, CA.

Reichelt, K. (1990). The Effect of a Gluten Free Diet on Glycoprotein Associated urinary Peptide Excretion in Schizophrenia. Journal of OrthomolecularMedicine, 5, 223- 239.

Rimland, B. (1988). Comparative Effects of Treatment on Child’s Behavior. Autism Research Review International, 2(4).

Sallows, G., & Graupner, T. (2001). Replicating the UCLA Model of Intensive Behavioral Treatment for Young Autistic Children: Results After Three to Four Years. Presented at the International Meeting for Autism Research (IMFAR), San Diego, CA., November 2001.

Seroussi, K. (2002). Unraveling the Mystery of Autism and Pervasive Developmental Disorder: A Mother’s story of Research and Recovery. New York, NY: Simon &Schuster.

Shattock, P., & Savery, D. (1997). Autism as a Metabolic Disorder. Autism Research Unit, School of Health Sciences. University of Sunderland, Sunderland, SR2 7EE,England.

Shaw, W. (2002). Biological Treatments for Autism and PDD.Lenexa, KS: William Shaw, Ph.D.

April 16, 2004

Faulty gene for bowel disease found

Filed under: News — luisa @ 10:16 am

Reported in the Globe and Mail on Monday, April 12, 2004

Canadian discovery, made public today, will help sufferers of painful Crohn’s, researchers say

By ANDRÉ PICARD
PUBLIC HEALTH REPORTER
Monday, April 12, 2004 – Page A6

Canadian researchers have isolated a gene that predisposes people to Crohn’s disease, a painful disorder that strikes young people and that has sharply increased in frequency in recent years.

The discovery will have an immediate impact, allowing researchers to distinguish more readily between Crohn’s and colitis, both inflammatory bowel diseases.

“The diagnostic benefits will be immediate,” said Katherine Siminovitch, a professor of medicine at the University of Toronto. “That’s important because you really want to catch these diseases in the early stages . . . then you can start a therapy that might put patients in remission and even eradicate the disease.”

Dr. Siminovitch said, however, that development of new drugs based on this genetic finding is a long-term prospect; new treatments are probably a decade away.

The research, published in today’s edition of the medical journal Nature Genetics, is nonetheless welcomed by people suffering from Crohn’s disease.

“This is an exciting event for us,” said Michael Howarth, executive director of the Crohn’s and Colitis Foundation of Canada.

“It’s important because it’s one more piece in the puzzle. Finding the cure is not likely going to be one big event, but come about by finding out a little more every year.”

More than 150,000 Canadians suffer from inflammatory bowel disease.

It most often strikes between the ages of 15-25, though a growing number of people are being diagnosed in their late 50s.

Crohn’s and colitis affect the digestive system and cause the intestinal tissue to become inflamed, form sores and bleed easily, leading to problems eating, bloody diarrhea and excruciating pain.

Most sufferers experience periods of remission and flare-ups of the disease, often requiring long-term medication, hospitalization or surgery.

Jessica Grossman, 14, of Toronto, was diagnosed as having Crohn’s five years ago. Since then, she has suffered greatly, enduring a number of drug treatments, all of which had severe side effects but none of which worked, and then surgery to remove her colon.

“It makes me happy to know they did this research because I don’t want other people to go through what I did,” Jessica said in an interview. She is currently in remission and remarkably healthy and active.

But Jonathan Grossman, Jessica’s father, said he is excited by the new finding.

“We’re quite cognizant of the fact that Crohn’s doesn’t just go away, so we really hope this will result in new treatments,” he said.

“Anything that alleviates the suffering of people with Crohn’s would be a godsend.”

Inflammatory bowel disease does not have a single cause but is believed to result from a combination of genetic and environmental factors, such as diet and exposure to disease. (When the body fights off disease, there is inflammation, and these diseases have their roots in inflammation gone awry.) The newly isolated gene is located on Chromosome 5.

It produces a protein that sits on the cell surface and regulates how substances enter and leave the cell. In a majority of Crohn’s disease patients, this protein functions improperly and allows in toxins.

Three years ago, French researchers discovered another abnormality, on Chromosome 16, that predisposes people to Crohn’s.

Dr. Siminovitch, who is also the founding scientist of Ellipsis Biotherapeutics Corp., said a person with both genetic abnormalities has a tenfold risk of developing Crohn’s disease.

She and her fellow researchers are now working on the development of a chemical that would alter the protein to restore its normal function. That chemical would become the basis of new drugs. The problem with drugs now being used to treat Crohn’s is that they are non-specific, and as a result have a lot of side effects.

Dr. Siminovitch said the findings could also shed light on the basic causes of chronic inflammation.

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