Transcript Dietary Intervention - Home | Early Intervention

Medina Blanchet, Dietetic Intern
Utah State University
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Autism first classified in 1943 by Dr. Leo
Kanner of Johns Hopkins.
1964 - Dr. Bernard Rimland of the Autism
Research Institute helped dispel “refrigerator
mother” theory.
1980 - became an official diagnosis, separate
from other conditions (1).
No clear etiology or cure. There is a genetic
link.
Some children can appear to be developing
normally until one or two years of age, with a
vocabulary of dozens of words, then within a
matter of weeks lose the ability to communicate and
become withdrawn.
During the 1990s, it was speculated that the
thimerosol in childhood vaccinations may have
caused autism.
Thimerosol has been used since the 1930s.
Numerous studies concluded that thimerosol
did not cause autism. However, in 2001 the
FDA decided to discontinue using it in routine
childhood vaccinations.
•Precaution
•Parents were refusing to immunize their
children.
Prevalence reports show that this did not slow
down the rise in the number of cases of autism
(2).
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Fall under the general category of Pervasive
Developmental Disorder (PDD).
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Autistic disorder
Asperger syndrome and
Pervasive developmental disorder – not otherwise
specified (PDD-NOS)
The American Psychiatric Association’s DSMIV specifies that child must have at least six
symptoms (from table) by age three for autistic
disorder.
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Children with Asperger syndrome are often
referred to as “high functioning”.
 No history of language delay
 Normal IQ
 The diagnosis for Asperger Syndrome is up to five
symptoms.
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PDD-NOS includes individuals with symptoms
who do not meet the criteria for the other
disorders and onset may occur after the age of
three (3).
DSM-IV List of Symptoms
Social Interaction
(minimum 2)
Marked impairment in the use of multiple nonverbal
behaviors
Failure to develop appropriate peer relationships (prefers
to be alone, little or no eye contact)
Lack of spontaneous seeking to share enjoyment,
interests or achievements with others
Lack of social or emotional reciprocity (not affectionate)
Communication
(minimum 1)
Delay or lack of development of spoken language
Marked impairment in ability to initiate or sustain
conversation
Repetitive use of language, such as echolalia (repeating
or phrases) or pronoun reversal
Lack of varied, spontaneous pretend or social imitative
play
Restricted repetitive, stereotyped behaviors, interests,
activities
(minimum 1)
Preoccupation with restricted patterns of interest with
abnormal intensity or focus (sustained odd play)
Apparently inflexible adherence to specific nonfunctional
routines or rituals (resists change)
Repetitive motor mannerisms (flapping, walking on toes)
Unusual interest in sensory things (lines things up, twirls
or flick objects, etc.)
Delays or abnormal functioning after the age of three
(minimum 1)
Social interaction
Language as used in social communication
Symbolic or imaginative play
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According to the CDC, ASDs occur in all racial,
ethnic and socioeconomic groups.
4x more likely to occur in boys than girls.
The average prevalence in the United States in
2009 was one in every 110 eight-year-old
children. (4)
The prevalence by state varies dramatically.
(See figure 1) (15).
Even more dramatic is the rate at
which ASD is increasing each
year. Over the past decade it has
increased over 500%.
(See figure 2) (16).
This rapid rise is an area of controversy.
Some experts believe it is due to an increase in
the rate of reporting officially diagnosed cases.
Sharon Lemons, RD is an officer for the Dietetics
in Development and Psychiatric Disorders
practice group with the American Dietetics
Association. She also has two sons with autism.
She states that early on parents did not want their
children diagnosed with autism because of the
negative stigma of “refrigerator mother” attached
to it.
As the diagnosis evolved, the stigma faded
and families were eligible for various
services.
Today, even very mild cases are being
diagnosed, which she believes could
account for the rapid rise in reported cases
(1).
Most likely, it is a combination of better
diagnostics and an increase in the incidence
of children being born with the disorder.
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Acknowledges that some families have found
that dietary intervention helps reduce the
symptoms of autism.
Until recently there has been no evidence from
controlled scientific studies to prove that to be
true.
It is recommended that families wishing to
pursue dietary intervention do so with the
guidance of a nutrition professional (5).
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GI disorders in ASD include GERD, abdominal
bloating, enzyme deficiencies, constipation, diarrhea
and inflammation of the GI tract and altered intestinal
permeability.
Non – GI issues include behavioral problems and
sleep disturbances.
Studies indicate these issues tend to be ↑ in ASD
children than in healthy age-matched controls.
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ASD children have a limited ability to communicate.
Very challenging to identify the source or location of
pain and discomfort. May manifest in behavior
problems and sleep disturbances. Inadequate sleep can
further aggravate behavior problems.
There is not sufficient scientific evidence to identify a
unique GI pathophysiology specific to ASDs (6).
Regardless, the GI disorders listed above can cause
maldigestion and malabsorption, which contributes to
nutrient deficiencies and food sensitivities.
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Occurs when the gut becomes inflamed.
Tight junctions holding the endothelial wall (gut
lining) together start to loosen, causing increased
permeability.
Allows foods to pass into the bloodstream from the
intestine before the food has been completely
broken down.
Partially digested food is not recognized by the
immune system. The immune system sends out
“the troops” known as antibodies to attack the
unknown food.
Anytime the immune system is activated, it causes
inflammation throughout the entire body.
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Fatigue
Headaches
“Foggy brain”
Rashes
Congestion
Sleep disturbances
Achy joints
Asthma
Ear infections, etc
Food that would normally have no
ill effects on a person with a
healthy gut can cause a whole host
of symptoms when the food is not
properly digested and absorbed.
(See figure 3)
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Broad category that includes food allergies and
food intolerances/sensitivities.
Food allergies are IgE mediated hypersensitive
reactions that occur within minutes of contact
with an allergen.
Once an IgE allergy has developed, it is often a
life-long condition. An example would be
developing anaphylaxis after eating peanuts.
Some hypersensitive reactions can be lifethreatening.
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Food intolerances are slow-reacting allergies
and are rarely life-threatening.
These sensitivities often resolve once the gut
heals.
Some laboratories use IgG antibody tests to
determine food intolerances.
Many in the allopathic medical community do
not consider these tests to be valid in the
clinical realm, but are useful in research (7).
The natural medicine community is more likely
to use this form of testing.
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IgG antibodies indicate that there has been
exposure to food.
They react significantly slower than IgE antibodies,
often taking days to manifest symptoms (7).
This makes it very difficult for a person to
recognize a food intolerance/sensitivity.
Research has shown that children with ASD have
higher amount of IgG antibodies to gliadin (part of
gluten) than those of the control group of healthy
children of the same age (8).
Anytime the immune system is activated,
inflammation results, regardless of the types of
antibodies involved.
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A clinical trial done in the late 90s studied 149
autistic children.
As much as 87% of the children had high titer IgG
antibodies to gliadin.
After being on a gluten-free/casein-free (GF/CF)
diet for 3 months 81% of the children showed
improvements.
This study included both physiological and
behavioral components.
The weakness of the study was that it was not
blinded. Behavioral results relied heavily on
parents and teachers who knew the children were
on a GF/CF diet (9).
An area of controversy with dietary
interventions in ASDs is the “parental
placebo effect”. Some researchers believe
that the extra attention given to the
children during a study may have more
influence on behavior than the dietary
intervention (10).
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“epi” means above
The study of how a person’s environment can
turn on or off genes.
At conception a person receives a genetic
blueprint, which cannot be altered.
Many factors influence whether a gene is
expressed or not, including development in
utero, early childhood development,
environmental pollutants, drugs, diet and
aging.
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If a person’s parents and grandparents both
have heart disease, there is a strong likelihood
that the person will inherit the gene for heart
disease.
This does not automatically mean that he/she
will develop the disease.
Many factors such as smoking, diet and
exercise will greatly influence the expression of
that gene.
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One of the ways the cells control which genetic
information they will use is by methylation.
Methyl groups are commonly found in the diet.
A methyl group is a carbon molecule and two
hydrogen molecules.
When this chemical modification process goes
haywire, hypermethylation can cause abnormal
expression or repression of genes.
(see figure 4) (11).
The National Institute of Mental
Health announced in its Science
News (December 2009) that
research has identified a silenced
gene which contributes to
aberrant social behavior in
autism (11).
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The study used postmortem brain tissue
samples from the temporal cortex of eight
autistic individuals.
Eight control samples were selected to match
patients on gender and age.
There was significantly more hypermethylation
of the oxytocin receptor in the autistic samples.
This genomic deletion silences that receptor.
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Not necessary to take brain tissue samples to
determine excess methylation of the oxytocin
receptor.
Methylation status can also be determined
from blood samples.
Has the potential to be used as a biomarker for
autism.
Epigenomic profiles undergo reprogramming
during very early gestation (12). Since early
detection and intervention are crucial, blood
tests done early in a child’s life, or even at
birth, may prove to have significantly more
impact on outcome.
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One of the most popular dietary interventions
for ASD children is a gluten-free/casein-free
diet.
Gluten is a protein found in wheat, barley and
rye.
It is a combination of two proteins – gliadin
and glutenin.
Gluten compromises 80% of the protein in
wheat. It provides elasticity, which makes
wheat flour the best grain for making bread.
Casein is a protein found in milk products.
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Proteins are large, complex molecules.
Gluten and casein seem to be particularly hard to
digest for many individuals.
Instead of being broken down into individual
amino acids, they are partially broken down into
peptides (several amino acids chained together).
Improperly digested and absorbed gluten/gliadin
and casein peptides can have an opiod-type effect
on the nervous system, interfering with
neurotransmission.
This is thought to contribute to behavior problems
in individuals with ASD. These dietary peptides
show up in the urine in abnormally high amounts
in autistic children (8).
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Clinical trials restricting gluten and casein are
difficult to conduct
due to the nature of ASD (behaviors causing dietary
challenges)
 dietary restriction of the study
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Of major concern are nutrient deficiencies as
the standard American diet consists of many
foods prepared with wheat products.
In Asian countries this is less of an issue as
their diets are mainly rice and vegetables.
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In 2010, a two-staged randomized controlled trial out
of Norway concluded that a GF/CF diet significantly
improved hyperactivity and attention deficit in
children with ASD.
72 Danish children were tested at baseline, 8 mo., 12
mo. and 24 mo.
Children were randomly selected to be in the diet and
non-diet groups.
Due to improvements in the diet group that exceeded
the researchers’ expectations, the non-diet group was
reassigned to the diet group at 12 mo.
The most dramatic results occurred in the first 8 mo of
the diet intervention. All study members, except the
nutritionists and the parents were blinded. A
weakness of the study was that they did not have a
placebo group (13).
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A smaller study done in Norway in 2002 looked at
the effects of dietary intervention in autistic
children with high urinary peptides.
These peptides originate as dietary gluten, gliadin
and casein.
Children were randomized into the GF/CF diet or
the control group.
The project leaders were blinded. The study lasted
for one year.
Results indicated that the diet group had
significant improvements in attention, social skills
and communication (14).
A weakness of this study is that it only involved a
total of 20 children.
In both of the Norwegian studies
researchers concluded that if
hyperactivity and/or attention
deficit were minimized, capability to
learn would improve.
Examples of other diseases/conditions that require dietary intervention:
Disease/Condition
Dietary Intervention
Cardiovascular disease Low saturated fat, low salt (TLC diet or DASH diet)
Kidney disease
Restrictions on protein, salt, potassium and phosphorus
Cystic Fibrosis
Type 2 diabetes
Increased fat, sodium, energy and extra digestive
enzymes
Low glycemic diet (45-60 carbs per meal)
PKU (Phenylketonuria)
Restrict phenylalanine (amino acid)
Celiac Sprue
No gluten (found in the grains wheat, barley and rye)
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In some disease states, dietary intervention or
medical nutrition therapy (MNT) can reduce
the incidence of complications, or slow the rate
of advancement.
Example - cardiovascular disease.
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Severe complications or even death can result
without dietary intervention
Example – PKU
A PKU diet is considerably more restrictive
than a GF/CF diet as phenylalanine is found in
almost all foods.
Newborn babies are routinely tested for PKU,
which is an inborn error of metabolism.
Early diet intervention can significantly reduce
brain damage.
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As researchers inch closer to finding the cause
of ASDs, it is apparent that something in the
diet may be a contributing factor to improper
gene expression via hypermethylation.
Further research is needed to determine
specific nutrients (or lack of nutrients),
chemicals or metabolic pathways that are
responsible for this aberration.
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Until the etiology is determined, early
detection and intervention can provide
significant reduction in the progression of the
disorder.
Now doctors depend on developmental signs
to make a diagnosis, making it very difficult to
do so before the age of one.
Hopefully soon, blood tests will be available to
detect abnormalities much earlier.
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A component of many GI disorders, especially
leaky gut.
When offending foods are eliminated,
inflammation subsides and the digestive tract
heals.
A healthy digestive tract digests and absorbs
nutrients as they were intended to be. The immune
system recognizes the “food” as safe.
This reduces systemic inflammation and resolves
or greatly reduces non-GI symptoms.
Diet intervention or MNT is
commonly used in many disease
states. The success of the outcome
is mostly dependent on adherence
to the diet. Guidance from wellqualified nutritionists can be very
helpful as families implement
dietary interventions.
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A GF/CF diet can reduce some of the signs and
symptoms associated with ASDs.
Gluten and casein are not found in vegetables,
fruits, meats, eggs, legumes, nuts, seeds and all
other grains, except wheat, barley and rye.
There can be small amounts of gluten in oats,
mainly due to cross-contamination.
It is possible to have a well-balanced GF/CF
diet.
Widespread use of flour in the standard
American diet - incorporating this diet can be
challenging.
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The most likely complication from strict dietary
interventions may be nutrient deficiencies.
Those may be remedied with appropriate and
consistent nutritional supplementation.
The ScanBrit study of 72 Danish children
mentioned earlier reported “no significant
adverse effects for any participant on [GF/CF]
diet intervention.” (13).
Families must decide for themselves if the
strictness of the intervention is worth the
reduction of the adverse manifestations of
ASDs.
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