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“….in many autistic children, bacterial and fungal overgrowths are etiologically significant in the cascade of events that result in autism or one of the other autism spectrum disorders.”
By Jaquelyn McCandless in Children with Starving Brains.
“A sensible and harmless form of warfare on the aberrant population of intestinal microbes is to manipulate their energy (food) supply through diet… By depriving intestinal microbes of their energy source, their numbers gradually decrease along with the products they produce.”
By Elaine Gottschall in Breaking the Vicious Cycle.
“Janie played with a doll for the first time ever today; I almost fainted. She initiated a hug and kiss for the first time ever in her 14 years of life.”
From Mom of Janie with Down’s syndrome, autism and gastrointestinal issues after a short time on the Specific Carbohydrate Diet.
The Specific Carbohydrate Diet has entered the world of autism through “the back door”- the intestinal tract. And what may have first appeared to be “the back door,” via the digestive system, is rapidly becoming one of the most scientifically researched areas in determining what may be one of the underlying causes of many autism spectrum disorders.
Because the Specific Carbohydrate Diet’s goal is to heal the intestinal tract and to rid it of bacterial and fungal overgrowth, it is proving to be a very successful dietary intervention in treating many autistic children and leading them back to a life of normalcy.
This chapter will review some of the research dealing with the Gut-Brain Axis in child developmental disorders. It will point out how dietary intervention with the Specific Carbohydrate Diet addresses and often overcomes conditions thought to be at the root of autism spectrum disorders as well as some cases of epilepsy and attention deficit disorder (ADD).
The previous chapter, The Brain Connection, highlights the research of many years in which it had been shown that various neurological problems originate in the digestive system. And when the number of autistic children soared within the last two decades, attention has again been directed to the gastrointestinal tract.
Parents of autistic children have always known that, among their children’s symptoms, there exists symptoms of chronic constipation, periods of diarrhea, and abdominal pain. But until recently, the parents’ reports were treated as of no consequence. Now, fortunately, attention is being focused on these physical symptoms as well as on behavior, and many gastroenterologists are in agreement that “these children are ill and are in distress and pain, and not just neurologically dysfunctional.” 1
Some physicians, recognizing that diet was playing a part in causing the intestinal symptoms focused their attention on treating these gastrointestinal symptoms as allergies and/or sensitivities. When testing these patients, they found evidence of sensitivities to various food components, mainly the gluten of grains and various components of dairy products.
The behavior of many autistic children, although not all,
showed improvement with the removal of these foods from
their diet but, unfortunately, although behavior often
improved, intestinal function did not. It was not unusual for
the author to receive letters from parents as follows:
“My son is almost six years old and has autism. He
was gluten/casein free for two years and while, during the
first six months I thought I saw improvement in his
exhibiting less stimmy (repeating the same action over
and over again), his stimming returned. Even while on
this diet, he still had constant stomach problems - being
hospitalized four times for throwing up and dehydration.
One time he suffered with a bowel obstruction; the other
times they weren’t sure what brought on his violent vomiting
attacks. No doctor even bothered to do a colonoscope.
I have mentioned to our doctor for years that he seems to
be addicted to potato chips, french fries, ketchup, and waffles.
When I learned of the Specific Carbohydrate Diet, it
addressed this carbohydrate addiction and I intend starting
this diet promptly.” “…Meanwhile, my younger child’s health was failing.
He was on a strict gluten-free diet because of celiac disease.
But it wasn’t helping. He was ghost white and rail
thin, with little energy and with chronic diarrhea and black
circles under his eyes. Deep down, I worried he was dying.
The team of pediatric specialists we were seeing had no
clue how to make my little boy healthy, nor did my daughter’s
“alternative” DAN (Defeat Autism Now) physician.
Fortunately, for us, this was August. And every doctor
treating my son was on vacation.
In desperation, I picked up a book called Breaking the
Vicious Cycle: Intestinal Health through Diet by Elaine
Gottschall. A stranger had mailed this book to me two
months earlier after meeting my Mother and hearing about
my son’s deteriorating health.
The book explained why my son wasn’t thriving on
the regular celiac diet. His intestines were so damaged he
couldn’t digest any grains, or complex carbohydrates. The
next day, he started the so-called Specific Carbohydrate
Diet (SCD) described in this book. His stools became normal,
and he started growing and gaining weight. He’s
now a strong, healthy seven-year old.
What about my daughter? She had no obvious digestion
troubles, but she did have “autism” and a recently
discovered yeast overgrowth. One British researcher
found a link between the MMR shot, intestinal problems,
and autism. Wouldn’t a diet that promised to heal her
intestines and help with yeast overgrowth be her best shot
at normal life?
We put Maria on a dairy-free version of the SCD. She
had a terrible yeast die-off that lasted a week even though
she was taking Nystatin, a popular antifungal drug. But
once she recovered from the die-off, about a week later, we
were confident she’d someday grow into an independent
adult, thanks to this remarkable diet. Her remaining
speech peculiarities, such as mixing up the order of words
in a sentence, disappeared. Her eye contact became normal.
By the time she was 4-1/2, one year after her diagnosis,
no one would guess she was ever “autistic.”
These parents’ reports are echoed throughout the
autistic community: although various dietary proteins appear
to aggravate behavioral symptoms, their removal is not
addressing the gastrointestinal problems. In addition it
becomes increasingly apparent that as a few dietary proteins
are removed, more and more must be taken out of the diet to
hopefully achieve and sustain progress until these children
have little to eat in the way of nutritious food. Parents continuously
complain of their children’s addiction to carbohydrates.
Dr. J. O. Hunter in 1991 described this dilemma of
treating patients with gastrointestinal symptoms as food
allergies or sensitivities. He stated that patients who exhibit
sensitivities do not follow classical Type I allergic reaction. If
these intolerances are not allergies, then they may be a disorder
of bacterial fermentation in the colon and the disorders
might be more appropriately named “enterometabolic (intestinal)
disorders.”2
The Specific Carbohydrate Diet approaches these gas-
trointestinal challenges in autism as it has been successfully
doing for inflammatory bowel disease - as a disorder of bacterial
fermentation and the ensuing problems which occur
because of bacterial fermentation. These problems resulting
from bacterial fermentation are: (1) production of excess
amounts of short chain volatile fatty acids (organic acids):
(2) lowering of the pH of the blood as these acids are
absorbed: (3) overgrowth of bacteria as the undigested carbohydrates
provide food for bacterial proliferation: (4) mutation
of some bacteria such as E. coli because of the change in
pH in their colonic environment; and (5) excess toxin production
caused by the overgrowth of some pathological bacteria.
Bacterial fermentation occurs when undigested carbohydrates
escape digestion and absorption and end up in the
lower parts of the small intestine and colon. Unlike diets that
eliminate only certain proteins, based on tests showing sensitivities
to proteins, and that allow unlimited intake of starches
and sugars, the Specific Carbohydrate Diet (SCD) is
designed to nourish the child optimally and to minimize bacterial
fermentation.
Coleman and Blass in 1985 in The Journal of
Developmental Disorders reported the first evidence that
autism might be linked to carbohydrate metabolism (digestion).
3 These researchers reported that the syndrome of Dlactic
acidosis was found to be present in autistic children.
Their work was based on reports of the 1970’s and 1980’s
showing that undigested carbohydrates were being changed
by bacterial action in the intestine to a substance, D-lactic
acid. High amounts of D-lactic acid in the bloodstream have
been found to cause bizarre behavioral symptoms. This book
discusses earlier research relating to D-lactic acidosis in
Chapter 7, The Brain Connection.4, 5, 6, 7, 8, 9, 10
There are two approaches to treating this abnormal
production of D-lactic acid: (1) use of antibiotics to kill the
bacteria producing the substance, a method often used med-
ically, and (2) decreasing the amount of fermentable carbohydrates
upon which bacteria feed in order to produce D-lactic
acid. Since antibiotic therapy often is accompanied by other
side effects, it seems reasonable to suggest dietary changes to
accomplish the same thing or as a support for medical intervention
with antibiotics.
The year 2000 yielded landmark research in linking
autism to the gastrointestinal tract. It was reported that
among 385 children on the autism spectrum, significant gastrointestinal
symptoms occurred in 46% compared with only
10% of almost 100 children without autism confirming what
parents already knew. 11
A flurry of remarkable scientific papers appeared, first,
in the British medical journal, Lancet12 and then in The
American Journal of Gastroenterology (Wakefield)13, demonstrating
conclusively that serious intestinal pathology was
found more than half of autistic patients. These intestinal
problems ranged from moderate to severe including esophagitis,
gastritis and enterocolitis along with the presence of lymphoid
nodular hyperplasia. Some of these intestinal pathologies
resembled Crohn’s disease as well as ulcerative colitis.
As would be expected, from previous research done on intestinal
problems (see pages 22-24), it was also found by
Horvath et al 14 that there was low carbohydrate digestive
enzyme activity (see diagrams of injured microvilli in the
chapter on Carbohydrate Digestion) although the pancreatic
function was normal.
Horvath’s report concluded by saying unrecognized
gastrointestinal disorders, especially reflux esophagitis and
disaccharide malabsorption, may contribute to the behavioral
problems of the non-verbal autistic patients.
Additional reports from findings at Harvard
Massachusetts General Hospital conclusively showed that carbohydrate
digestion is being hampered at the locus of the
intestinal absorptive cell.15
Initial autism research findings at Harvard
Massachusetts General testing 400 autistic children found
that (1) lactase deficiency was found in 55% of ASD children
tested; (2) combined deficiency of disaccharidase enzymes
was found in 15%; and (3) enzyme assays correlate well with
hydrogen breath tests. (The hydrogen breath test measures
the amount of hydrogen gas given off when intestinal
microbes ferment unabsorbed carbohydrates.)
This current work, on decrease in digestibility of
dietary disaccharides leading to malabsorption, forms the
basis for therapy of the Specific Carbohydrate Diet. Its goal is
to keep disaccharide ingestion to a minimum by avoiding lactose,
sucrose, maltose and isomaltose (remnants of starch
digestion) and to provide a nutritious, healing diet without
these double sugars and to deprive the microbial world of the
intestine from a surplus of fermentable carbohydrates.
It is well known that compounds arising in the intestinal
tract can enter the bloodstream and cross the blood brain
barrier.16 (Gastroenterologists have been aware of this in
treating the neurological effects of liver disease, hepatic
encephalopathy. Reports have been published on how these
toxins from the intestinal tract affect neurotransmitter substances
in the brain.17 Other research by E.R.Bolte18 in an
effort to correlate autism behavioral symptoms to the intestinal
tract, investigated how the toxin of one bacterium,
Clostridium tetani, could find its way from the intestinal tract
to the central nervous system via the vagus nerve.
But there is still disagreement among researchers as to
what constitutes the toxins from the gastrointestinal tract and
what their origins are. Again, are they derived from proteins
or are they products of intestinal bacterial action? This question
was addressed in an outstanding research paper published
in Neuropsychobiology in 2002 and authored by Dr.
Harumi Jyonouchi et al.19 Dr. Jyonouchi’s group were the first
to explain how bacterial toxins from the intestine can result in
sensitivities to certain dietary proteins, and casts light on the
conundrum of which comes first: allergies/sensitivities which
might lead to intestinal inflammation, or bacterial and yeast
overgrowth (infections) which can lead to sensitivities to certain
dietary proteins. The question can be viewed as “can the
body’s innate immune system, by reacting to the toxins of
certain bacterial cell walls, cause the sensitivities to proteins
such as casein and gluten?” The authors suggest that the root
cause of the food protein sensitivity may be an underlying
sensitivity to endotoxin, which arises from the surfaces of
gram-negative bacteria in the gut flora: the lipopolysaccharide
component of the cell wall of certain bacteria present in
the intestine.20
This response to an endotoxin of intestinal bacterial
cells is considered an innate immune response, an ancient
form of defense and coded in the genes as an inherited trait.
This innate immune response to the bacterial toxin could
stimulate the production of antibodies and cytokines, initiators
of an inflammatory response, part of an adaptive immune
response.21 Dr. Jyonouchi’s research is an attempt to answer
the question of why there is gastrointestinal pathology in children
exhibiting autism spectrum disorders and invites the
research community to explore dietary intervention in order to
ameliorate the behavioral symptoms of autism.
It is the hope of the author that this book will be of
help to the research community in understanding how the
molecular components of commonly eaten foods affect this
problem and how changing the child’s diet can, indeed, break
the vicious cycle. Important note to parents of autistic children:
When implementing The Specific Carbohydrate Diet, it
is important to remember that during the first week to ten
days, profound changes are occurring in the digestive tract:
the hundreds of different families of microorganisms are
changing their metabolic functions due to the lack of nutrients
to which they have been accustomed and of which they are
now being deprived Some children may do well even during
the first week. But others will go through a period of adjustment
which some refer to as “detoxification.” It will be helpful
during this period to find support from the many other
parents who have been through this change. Going to the following
websites can give you this support.
It is especially important that you read the information
on these websites relating to the introduction of dairy products.
A decision can then be made if the Specific
Carbohydrate Diet should be implemented with or without
dairy.
And another letter from Patricia :
BreakingtheViciousCycle.info
Footnotes:
1. Buie, T., H. Winter and R. Kushak. 2002. Preliminary findings
in gastrointestinal investigation of autistic patients.
2. J.O. Hunter. 1991. Food allergy or enterometabolic disorder.
Lancet 338: 495-496.
3. Coleman, M. and J.P. Blass. 1985. Autism and lactic acidosis.
Journal of Autism and Developmental Disorders. 15:1-8.Four
patients are described who have two coexistent syndromes: the
behavioral syndrome of autism and the biochemical syndrome
of lactic acidosis. One of the four patients also had hyperuricemia
and hyperuricosuria. These patients raise the possibility
that one subgroup of the autism syndrome may be associated
with inborn errors of carbohydrate metabolism.
4. Man S. Oh, K.R. Phelps, M. Traube, J.L. Barbosa-Salvidar, C.
Boxhill, and H.J. Carroll. 1979. D-lactic acidosis in a man
with the short-bowel syndrome. The New England Journal of
Medicine 301:249-252.
5. Stolberg, L., R. Rolfe, N. Gitlin, J. Merritt, L. Mann, Jr., J. Linder,
and S. Finegold. 1982. D-lactic acidosis due to abnormal flora.
The New England Journal of Medicine 306:1344-1348.
6. Perlmutter, D.H., J.T. Boyle, J.M. Campos, J.M Egler, and J.B.
Watkins, 1983. D-lactic acidosis in children: an unusual
metabolic complication of small bowel resection. The Journal
of Pediatrics 102:234-238.
7. Haan, E., G. Brown, A. Bankier, D. Mitchell, S. Hunt, J. Blakey,
and G. Barnes. 1985. Severe illness caused by the products of
bacterial metabolism in a child with a short gut. European
Journal of Pediatrics 144:63-65.
8. Traube, M., J. Bock, and J.L. Boyer. 1982. D-lactic acidosis
after jenunoileal bypass. The New England Journal of
Medicine 307:1027.
9. Mayne, A.J., D.J. Handy, M.A. Preece, R.H. George, and I.W.
Booth. 1990. Dietary management of D-lactic acidosis in short
bowel syndrome. Archives of Diseases of Childhood 65:229-
231.
10. Thurn, J.R., G.L. Pierpont, C.W. Ludvigsen, and J.H. Eckfeldt.
1985. D-lactate encephalopathy. The American Journal of
Medicine 79:717-721.
11. Melmud, R., C. K. Schneider, R. A. Fabes, et al.
2000.Metabolic markers and gastrointestinal symptoms in chil-
dren with autism and related disorders. Journal of Pediatric
Gastroenterology and Nutrition. 31:A116.
12. Wakefield, A.J., S. H. Murch, A. Anthony, J. Linnell, D. M.
Casson, M. Malik, M. Berclowitz, A.P. Dhillon, M. A. Thomson,
P. Harvey, A. Valentine, S.E. Davies, and J. A. Walker-Smith.
1998. Ileal-lymphoid-nodular hyperplasia, non-specific colitis,
and pervasive developmental disorder in children. Lancet 351:
637-41.
13. Wakefield, A.J., A. Anthony, S.H. Murch, M. Thomson, , S.M.
Montgomer, S. Davies, J. J. O’Leary, m. Berelowitz, and J.A.
Walker-Smith. 2000. Enterocolitis in children with developmental
disorders. American Journal of Gastroenterology
95:2285-2295.
14. Hovarth, K., J.C. Papadimitriou, A. Rabsztyn, C. Drachenberg,
and J. T. Tildon. 1999. Gastrointestinal abnormalities in children
with autistic disorder. Journal of Pediatrics 135: 559-63.
15. Harvard Autism Project. 2002. Initial Autism Research
Findings at Harvard Massachusetts General Hospital.
16. Wakefield, A. J. 2002. The gut-brain axis in childhood developmental
disorders. In Journal of Pediatric Gastroenterology
and Nutrition. Lippincott Williams & Wilkins, Inc.,
Philadelphia.
17. Butterworth, R. F. 2000. Complications of cirrhosis III hepatic
Encephalopathy. Journal of Hepatology 32:171-180.
18. Bolte, E. R. 1998. Autism and Clostridium tetani. Medical
Hypothesis 55:133-44.
19. Jyonouchi, H, S. Sun, and N. Itokazu. 2002. Innate immunity
associated with inflammatory responses and cytokine production
against common dietary proteins in patients with autism
spectrum disorder. Neuropsychobiology 46:76-84.
20. Ulevitch, R.J. and P.S. Tobias. 1999. Recognition of gramnegative
bacteria and endotoxin by the innate immune system.
Current Opinions Immunology. 11:19-22. Until about 10 years
ago the exact mechanisms controlling cellular responses to the
endotoxin – or lipopolysaccharide (LPS) – of Gram-negative
bacteria were unknown. Now a considerable body of evidence
supports a model where LPS or LPS-containing particles
(including intact bacteria) form complexes with a serum protein
known as LPS-binding protein; the LPS in the complex is
subsequently transferred to another protein which binds LPS,
CD14. The latter is found on the plasma membrane of most
cell types of the myeloid lineage as well as in the serum in its
soluble form. LPS binding of these two forms of CD 14
results in the activation of cell types of myeloid and nonmyeloid
lineages respectively.
21. Medzhitov, R. and C. Janeway. 2000. Innate immunity. The
New England Journal of Medicine 343:338-344.