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Intl. J. of Molecular Zoology, 2012, Vol.2, No.1, 1
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http://ijmz.sophiapublisher.com
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Research Report Open Access
The Role of Breastfeeding and the Intake of Bovine Colostrum in Autistic
Neonatal Rats with Coeliac Disease
Manar E. Selim
1
, Laila Y. Al-Ayadhi
2
1. Zoology Department, Faculty of Science, King Saud University, Autism Research and Treatment Center, AL-Amodi Autism Research Chair, Riyadh,
Kingdom of Saudi Arabia
2. Physiology Department, Faculty of Medicine, King Saud University, Autism Research and Treatment Center, AL-Amodi Autism Research Chair, Riyadh,
Kingdom of Saudi Arabia
Corresponding authors email: manar.selim@hotmail.com;
Authors
International Journal of Molecular Zoology, 2012, Vol.2, No.1 doi: 10.5376/ijmz.2012.02.0001
Received: 02 Apr., 2012
Accepted: 04 Apr., 2012
Published: 28 Apr., 2012
This is an open access article published under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction
in any medium, provided the original work is properly cited.
Preferred citation for this article:
Selim et al., 2012, The Role of Breastfeeding and the Intake of Bovine Colostrum in Autistic Neonatal Rats with Coeliac Disease, Intl. J. of Molecular Zoology,
Vol.2, No.1 1
-
12 (doi: 10.5376/ijmz.2012.02.0001)
Abstract
Autoimmune deficiencies are linked to Autism Spectrum Disorder. Coeliac Disease (CD), also known as an auto-immune
disease since IgG and IgA antibodies produced by the immune system against specific gluten components, namely gliadin, also target
and damage the intestinal tissue, resulting in the characteristic deformed villi which impairs absorption of nutrients. Bovine
colostrums are the first milk produced postpartum, and are typically defined as the first six postpartum milkings collected during the
period of transition from colostrums to milk. This commentary discusses the role of breastfeeding and the intake of colostrum to
overcome coeliac disease in autistic neonatal rats.
Keywords
Autism; Breastfeeding; Coeliac disease; Bovine colostrums
Introduction
Coeliac disease (CD), which develops in genetically
susceptible individuals after ingestion of gluten-
containing food, is characterized by damaged intestinal
mucosa with malabsorption of most nutrients (Marsh,
1992). The disorder, which affects the proximal small
intestine, is characterized by crypt cell hyperplasia and
villus atrophy. The active component of wheat gluten
is a complex mixture of glutamine- and proline-rich
proteins called gliadin (Kasarda, 1997). A significant
association between maternal history of Coeliac
disease and ASDs was observed for the first time
(Norgard et al., 1999). The observed associations
between familial autoimmunity and ASDs/infantile
autism are probably attributable to a combination of a
common genetic background and a possible prenatal
antibody exposure or alteration in fetal environment
during pregnancy (Ludvigsson et al., 2005). In a more
recent publication (Wakefield et al., 2008), it was
observed that ileal LNH (lymphoid nodular
hyperplasia) presented in 93% of affected children
with autism and 14.3% of control children. Colonic
LNH was present in 30% of affected children and
5.4% of control children. Hyperplasia of the
intestinal lymph nodes was found in 88.5% of biopsies
of affected children. Active inflammation of the ileum
(ileitis) and duodenum was observed in 88% and
chronic inflammation of the colon (colitis) was seen in
8% of affected children. The authors characterized the
pathology as “a subtle new variant of inflammatory
bowel disease that lacks the specific diagnostic
features of either Crohn’s disease or ulcerative
colitis.” In yet another study (Horvath et al., 1999)
used endoscopy with biopsy to examine the upper GI
tract of 36 children diagnosed with autism and
experiencing abdominal pain, chronic diarrhea,
bloating, nighttime awakening, or unexplained
irritability. Abnormal findings included reflux
esophagitis in 25 of the children, chronic gastritis in
15, and chronic duodenitis in 24. Low activity of
intestinal carbohydrate digestive enzymes was
observed in 21 children, whereas 27 exhibited
increased exocrine secretion of pancreatic-biliary fluid
after intravenous administration of the GI hormone
secretin. Secretin, a peptide hormone released by
endocrine cells within the duodenal mucosa, promotes