ArticlePDF Available

Autism spectrum disorder: A review of the current understanding of pathophysiology and complementary therapies in children


Abstract and Figures

Autism is a complex condition which affects speech, language, neurodevelopment, sensory perception and social interaction. Until recently the pathophysiology of this condition has been poorly understood. Immunological and neurological research in autistic patients has improved the understanding of autism greatly. It is important that this research filters through to clinical practice, so that appropriate therapies may be employed. Autism requires a multidisciplinary approach to maximise the potential of patients affected by it. As such, it is important that different models of care support each other and do not place undue stress on the patient. Natural therapies can play a key role in supporting the outcomes of other therapies such as psychology, occupational therapy and speech therapy, and by doing so, improve lifelong outcomes.
Content may be subject to copyright.
Australian Journal of Herbal Medicine 2013 25(3)
128 © National Herbalists Association of Australia 2013
Autism Spectrum Disorder (ASD) is a developmental
disorder which affects language development, social
interaction and communication and involves restrictive
and repetitive areas of interest and behaviours (London
2007). It is a spectrum of disorders which includes
Asperger’s Disorder, Disintegrative Disorder, Pervasive
Developmental Disorder Not Otherwise Specied (PDD-
NOS) and Atypical Autism (Meletis 2007). Diagnosis
involves a multidisciplinary team, which includes
assessment of verbal and nonverbal communication,
adaptive behaviours, atypical behaviours, ne and gross
motor skills and cognitive status (Samtani 2011). The
ways in which this presents in children vary signicantly.
The Diagnostic and Statistical Manual of Mental
Disorders (DSM-V) has recently replaced DSM-IV.
Autism Spectrum Disorder is now an umbrella diagnosis,
as opposed to being differentiated into different categories.
The main criticism of the previous diagnostic criteria
(DSM-IV) is inconsistency of diagnosis (Kaufmann
2012). Previously Asperger’s Disorder (AD) was
differentiated from High Functioning Autism by the lack
of language delay (Entiticotti 2010). There is however
no pathophysiological differentiation between these
two categories (Kaufmann 2012). The new diagnostic
schedule attempts to simplify the diagnosis and encourage
the diagnosing physician to include a description of the
key areas of difculty for each individual, thus giving
clarity to individual variation within the spectrum (Table
1). This description would include: details regarding the
severity of ASD symptoms; verbal abilities; the pattern
of onset; clinical progression; etiologic factors; cognitive
abilities (IQ); and associated conditions or co-morbidities.
It is hoped that the new diagnostic criteria will simplify
access to services for children with ASD and that the
diagnostic report will give more specic information to
other therapists involved in the co-management of a child
with ASD (Kaufmann 2012).
Table 1: Current diagnostic criteria for autism
spectrum disorder
Kaufmann WE. DSM-V: The New Diagnostic Criteria for Autism
Spectrum Disorders. Department of Neurology Boston Children’s
Hospital, Harvard Medical School.
Currently, or by history, must meet criteria A, B, C, and D
A. Persistent deficits in social communication and social
interaction across contexts, not accounted for by general
developmental delays, and manifest by all 3 of the following:
1. Deficits in social-emotional reciprocity
2. Deficits in nonverbal communicative behaviours used
for social interaction
3. Deficits in developing and maintaining relationships
B. Restricted, repetitive patterns of behaviour, interests, or
activities as manifested by at least two of the following:
1. Stereotyped or repetitive speech, motor movements,
or use of objects
2. Excessive adherence to routines, ritualized patterns of
verbal or nonverbal behaviour, or excessive resistance
to change
3. Highly restricted, fixated interests that are abnormal in
intensity or focus
4. Hyper- or hypo-reactivity to sensory input or unusual
interest in sensory aspects of environment
C. Symptoms must be present in early childhood (but may
not become fully manifest until social demands exceed
limited capacities)
D. Symptoms together limit and impair everyday functioning.
Autism spectrum disorder: A review of the
current understanding of pathophysiology and
complementary therapies in children
Belinda Robson
Goulds Naturopathica, Hobart, Tasmania
Abstract: Autism is a complex condition which affects speech, language, neurodevelopment, sensory perception and social
interaction. Until recently the pathophysiology of this condition has been poorly understood. Immunological and neurological
research in autistic patients has improved the understanding of autism greatly. It is important that this research filters through to
clinical practice, so that appropriate therapies may be employed. Autism requires a multidisciplinary approach to maximise the
potential of patients affected by it. As such, it is important that different models of care support each other and do not place undue
stress on the patient. Natural therapies can play a key role in supporting the outcomes of other therapies such as psychology,
occupational therapy and speech therapy, and by doing so, improve lifelong outcomes.
Australian Journal of Herbal Medicine 2013 25(3)
129© National Herbalists Association of Australia 2013
The diagnosis of ASD has rapidly increased over the
last 20 years. In the early 1990s prevalence of ASD in
western countries was estimated at 1 in 1000. In 2002
rates of autism have been reported as 1 in 150 (6.6 in
1000). Other authors report incidence at 1.5-2% (i.e.
15-20 in 1000). Rates vary geographically and are
reported differently. For example, there has been lower
prevalence reported in Alabama with 3.3 per 1000 8-year
olds diagnosed with ASD, compared to New Jersey
with 10.6 per 1000 8-year olds. Furthermore, rates of
autism seem to be rising faster than can be explained by
improved diagnosis (London 2007).
Why are the rates of autism increasing?
Current research suggests that prenatal factors
signicantly inuence the incidence of ASD. Prenatal
exposure to rubella or cytomegalovirus greatly increases
the risk for autism (Patterson 2009). It has been estimated
that if viral (inuenza, Herpes simplex virus, rubella),
bacterial (urinary tract) and parasitic (toxoplasma)
infections could be prevented in pregnant women, >30% of
schizophrenia cases could be prevented (Patterson 2011).
This research is relevant when looking at prenatal ASD
risk, in that schizophrenic patients show similar cytokine
dysregularity and that this dysregularity remains in the
offspring through childhood into adulthood (Patterson
2011). Increased rates of positive reactivity for several
serum antibodies to specic CNS proteins have been
observed in children with autism, specically affecting
the basal ganglia, the frontal lobe, the cingulate gyrus
and the cerebellum (Zimmerman 2007). Interleukin-6
(IL-6) has been implicated in pathogenic changes to
brain development in vivo (Smith 2007). IL-6 interferes
with transcription pathways that regulate neurogenesis
and gliogenesis (Smith 2007). Additionally other
studies, both animal and human, have demonstrated the
production of maternal antibodies which interfere with
prenatal brain development (Zimmerman 2007). These
immunological patterns in-utero may be responsible
for altered serum reactivity and other immune system
dysregularity observed in children and adults with ASD
(Zimmerman 2007).
Advanced maternal and paternal age has also been
associated with increased incidence of ASD (Croen
2007). While studies looking at the inuence of maternal
and paternal age are not consistent, a 2009 meta-analysis
found that each independently increased the incidence
of ASD (Gardener 2009). One study suggested that, if
parental age is causal, 4-13% of ASD cases could be
attributed to parental age being >35 years (Croen 2007).
While many independent prenatal factors are associated
with increased incidence of ASD, the current understanding
is that no single factor is causative. Genetics may also have
a big part to play. Parents with one ASD child have a 27%
chance of having subsequent children with ASD (Tomeny
2012). The current thinking is that genetics create a
predisposition, and prenatal factors inuence the likely
expression of those genetics and the severity of impact
on the child. In a clinical setting, these trends highlight
Table 2: Maternal factors associated with increased ASD incidence
Maternal history Maternal Tertiary education Croen 2007
Previous foetal loss Gardener 2009
Atopic disease (40% of mothers of children with ASD have some kind of allergy) Mostafaa 2008
Vitamin D deficiency Nagwa 2010,
Fernell 2010
Prenatal factors Twofold increase in incidence of autism in children whose mothers used an SSRI
(Selective Serotonin Reuptake Inhibitor) antidepressant in the year prior to delivery
Croen 2007
Peri-natal factors Induction of labour Juul-Dam 2001
Labour <3 hours Juul-Dam 2001
Prolonged labour >20 hours Gardener 2009
Pre-eclampsia Gardener 2009
Maternal hypertension Gardener 2009
Oxygen required at birth Gardener 2009
Rhesus incompatibility Gardener 2009
Almost fourfold increase in incidence with SSRI antidepressant use in first trimester Croen 2007
Birth order 1st born and 4th or subsequent children Tomeny 2012
Infant feeding Absence of breastfeeding Al-Farsi 2012
Reduced period of exclusive breastfeeding Al-Farsi 2012
Late initiation of breastfeeding (no colostrum) Al-Farsi 2012
Early weaning Al-Farsi 2012
Australian Journal of Herbal Medicine 2013 25(3)
130 © National Herbalists Association of Australia 2013
the importance of preconception care, particularly as the
average age of childbearing increases and more so in
couples with a family history of ASD or atopy.
Specic physiological and biochemical differences
have been observed in people with ASD that are pertinent
to the therapist’s understanding of autism and have
bearing on clinical treatments and outcomes.
Hyperserotonemia has been observed in 25-40%
of children and adolescents with autism (Aldred 2003,
Kidd 2003). Dopaminergic imbalances are also common,
with likely dopamine insufciency in CNS (Kidd 2003).
Imbalances in serotonin and dopamine will inuence
prevalence of anxiety and depression in people with
ASD, and should be considered during the assessment
process. Reduced γ-Aminobutyric Acid (GABA) proteins
have also been observed in people with autism, as well
as down regulation of GABA receptors (Fatemi 2010,
Fatemi 2009). GABA is involved with inhibitory actions
in the brain.
Signicant differences in brain structure and
functionality have been observed via magnetic resonance
imaging and autopsy in children with autism as detailed
in Table 3.
To put it simply, the brain is structured differently in
individuals with autism. While ASD affects many systems
within the body it is also a neurological disorder. Many of
the challenges that people with autism face, such as social
difculties, language difculties, sensory issues and
processing speed, directly relate to these differences in the
way the brain is structured and how it communicates with
other areas of the brain. Altered balance of local and global
connectivity in the autistic brain may lead to development
of prodigious skills coexisting with impaired executive
function and social cognition (Takahata 2008). This may
present as enhanced memory skills or exceptional skills
in xed areas of interest. Global connectivity between
prefrontal cortex and other areas of the brain may explain
cognitive impairments, impulsivity and restriction of
interests (Takahata 2008). Reduced neuron recruitment
could explain slower processing speed and transition
difculties (Agam 2010, Kenet 2012). This may also
explain exam difculties where autistic students focus
intensely on early exam questions at the expense of the
rest of the exam.
Oxidative stress and inflammation
People with ASD also exhibit raised biochemical
markers for lipid oxidation and inammation. Lipid
peroxides are signicantly raised, as are urinary
isoprostanes. Lipofuscin in the cortical brain is elevated,
which is a marker of oxidative tissue damage. Lower
levels of antioxidants (both enzymes and nutrients) have
been observed in autistic patients. This includes lower
levels of total plasma glutathione, plasma vitamins C, E,
A, and red-cell selenium (McGinnis 2004).
Higher levels of inammation and free radical
production have been observed in autistic patients, both
in the gastrointestinal system and the brain. Inammation
in the gastrointestinal system raises cytokine production
systemically, which in turn promotes a hyper-permeable
blood-brain-barrier, apoptosis, neurodegeneration and
demyelination (McGinnis 2004).
Allergies and gastrointestinal hyper-
Increased gastrointestinal permeability is also
common in people with ASD. Food allergy and
intolerance is common and may be the underlying
cause of gastrointestinal hyperpermeability or may be
consequential. The C4B null allele is present in 42%
children with autism, which predisposes for autoimmune
and allergic development (Mostafaa 2008). Lactase
deciency may be present in up to 58% of children with
ASD ≤5 years old (Kushak 2011). Furthermore, a 2008
study found 52% of children with autism had some kind
of allergic disease, and that children with gastrointestinal
symptoms and ASD had an 88% chance of allergic
Table 3: Neurological and functional differences observed in children with ASD
Decreased cerebellum size Wagner 2006
Altered number of Purkinje cells Wagner 2006
Altered hippocampus size and cell number Wagner 2006
Overall brain size is greater, with increased neurons in cerebral cortex Vaccarino 2009
Decreased activity in temporal lobe Wagner 2006
Basal ganglia show structural changes and functional impairment Wagner 2006
Reduced connectivity between the cortical ocular motor control network Kenet 2012
Reduced neuron recruitment to prepare for task difficulty Kenet 2012
Changes to dopaminergic and serotonergic activity in the striatum Wagner 2006
Up to 40% have raised serotonin levels Kid 2003
Dopaminergic imbalances are common, with likely dopamine insufficiency in CNS. Kid 2003
Australian Journal of Herbal Medicine 2013 25(3)
131© National Herbalists Association of Australia 2013
disease (Mostafaa 2008). Understandably, malabsorption
syndromes are common, particularly when there is an
underlying food allergy/intolerance that has not yet been
identied or effectively eliminated. Abdominal pain,
discomfort, bloating, diarrhoea, anorexia and other signs
of gastrointestinal upset should be assessed. In autistic
children who are nonverbal this may be difcult to assess.
Additionally they may have had these symptoms for so
long that they do not understand that this is not normal.
Other manifestations of atopy such as hay fever, asthma,
eczema and allergic rhinitis should also be assessed.
Family and social context
In treating a child with ASD one must also consider
the family context. Recent studies have examined the
implications of ASD on other siblings within the family.
Neurotypical children with an older sibling with ASD
are more likely to exhibit higher levels of behavioural
difculties or language delay, and other subclinical
characteristics of ASD (Tomeny 2012, Constantino
2010). Stress levels within the home in these families can
be extreme and in such situations the role of adaptogens
should not be underestimated. Various television
programs have popularised a very bleak picture for
families of autistic children, suggesting divorce rates of
80- 85% (Winfrey 2007, Lofholm 2008). While these
gures are alarming, they are not consistent with recent
studies (Higgins 2005, Hartley 2011, Mailick-Seltzer
2011, Naseef 2012, Baeza-Velasco 2013).
A study conducted at the University of Wisconsin in
2010 compared data collected from 406 adolescents and
adults living with ASD to the national standard (Hartley
2011). This study found that 23.5% of parents having a
child on the spectrum separated, compared to the national
average 13.8% (Hartley 2011). Similarly a 2013 study
of 119 families in Victoria, Australia reported a 25.2%
separation rate in parents with an ASD child (Baeza-
Velasco 2013). Furthermore the Wisconsin study found
that whilst in families without a child with a disability
the divorce rate tends to decline once the child is over 8
years old, it remains high in couples with an autistic child
(Hartley 2011). The authors speculate that while family
stress levels are highest in most families while a child
is quite young, these pressures become less as the child
becomes more independent. In families with an ASD
diagnosis this reduction in stress levels does not occur.
Many people with ASD continue to need support
well into adulthood and as such family stress levels
may remain high for a much longer period of time. A
2012 study stated that seventy-ve percent of people
with autism will require lifelong educational and social
support (Mefford 2012). Consequently, parents of
children with ASD experience worry and anxiety for
their offspring for much longer periods of their lives
and lack the surety that their child will be able to live
a fullling and independent life. Providing support for
parents using stress management strategies thus becomes
part of the natural therapist’s role in the treatment of a
child with autism.
Barriers to diagnosis
Reluctance to “label” often may become a stressor
that divides parents and is in itself a limitation to starting
effective treatment. Possibly with the exception of
regressive cases of autism, signs are usually present very
early in a child’s life (Teirney 2004, Matson 2012). Eighty
percent of parents have reported some concern about a
child’s development by 18 months old and diagnosis
usually occurs between 2 ½ - 4 ½ years old (Mundkur
2005). Early intervention strategies, including speech and
occupational therapy, utilise the increased neuroplasticity
that is present in very young children. Neuroplasticity, the
ability of the brain to develop new neuron connections in
response to stimuli or experience, is greatest for visual
stimuli before the age of seven years, and greatest for
language acquisition before age six years (Mundkur
2005). Current research suggests that early intervention
helps to minimise the severity of lifelong symptoms
(Teirney 2004, Matson 2012). The importance of the role
of the health professional in facilitating early diagnosis
cannot be overstated. Dismissing a parent’s concern may
be harmful in that it delays assessment of the child and
subsequently delays access to support and therapies.
Parents and teachers are the best placed people to identify
problems that a child may be having. It is imperative that
their concerns be taken seriously so as not to lose a critical
therapeutic window for neurodevelopment.
Speech delay and language difficulties
Where speech delay is absent, people with ASD are
likely to have disorganised or very unusual language,
or may speak monologues in specic areas of interest
(Woodbury-smith 2009). Echolalia is often used as
means to communicate and is typically more advanced
in children without a language delay. Echolalia is most
simply described as a cut and paste strategy for learning
language. Rather than learning how to put individual words
together and formulate a response to a question, the child
learns phrases or sets of words that can be memorised and
effectively used to respond to particular questions. These
phrases or sets of words are often learnt from dialogue on
television or from peers or parents. These phrases may
make learnt responses unusual. They may have limited
or repetitive responses and may not answer at all if the
question is one to which they do not know how to respond.
A speech stutter is also common in people with ASD and is
more likely when anxiety is also a problem (Davis 2011).
Language comprehension is also limited in that
language processing is very literal (Law 1995). This is
often perceived as a lack of sense of humour in the ASD
child, as they have difculty differentiating sarcasm and
untruths from normal conversation. They often have
difculty with making and keeping eye-contact with
other people and have marked difculty observing and
Australian Journal of Herbal Medicine 2013 25(3)
132 © National Herbalists Association of Australia 2013
interpreting differences in body language and facial
expressions. Socially this makes them vulnerable to
being the butt of jokes or school yard pranks and creates
a certain gullibility that if not careful, can be exploited.
Colloquial phrases also create difculty, because they do
not make literal sense. Children are told “pull your socks
up,” or “jump into bed,” and may interpret this literally.
For children with ASD this creates further frustration and
confusion, particularly if they are chastised for doing
literally what they are told.
Processing auditory language can be particularly
difcult (Law 1995). Children on the autism spectrum
are often visual learners. In a classroom setting this
creates difculty if the teacher relies heavily on verbal
instruction. These children benet greatly from visual
teaching methods. Predicting sequential activities
throughout the day can also be particularly difcult for
people with ASD, even if the routine is well established.
A simple but effective strategy for this is the use of a
visual schedule. A visual schedule can be a list, in pictures
or words, that lets the child know what to expect, and
greatly reduces anticipatory anxiety (Curtis 2010).
Co-morbidities are common in children with ASD
and may also need specialist attention (Table 4) (Matson
2009). It is important to consider the relevance of these
co-morbidities, what they tell us about the individual
challenges for the patient and the impacts they have on the
patient and their family. Sleep disorders are common. In
ASD patients there has been observed a genetic difculty
in melatonin synthesis (Golink 2010). This presents
as difculty getting to sleep and staying asleep, with
obvious secondary impacts on daytime alertness, mental
function and coping skills. Depression and anxiety are
also common, which is likely explained by alterations
in levels and responsiveness to serotonin and dopamine
(Kidd 2003). Obsessive-compulsive disorder may also be
co-diagnosed, though it is arguable that being obsessive
about xed areas of interest is part of being autistic.
Lack of ability to maintain attention, or symptoms of
hyperactivity (as in ADHD) are also within the scope
of ASD, and suggest that there are sensory processing
issues that need further addressing.
Sensory Processing Disorder (SPD)
Sensory Processing Disorder (SPD) is a common
feature of ASD. SPD refers to the process of receiving
sensory messages by the nervous system and the
conversion of those messages into responses (Miller
2006). In people with SPD the brain lacks the ability
to lter out all the background sensations. In SPD one
or more of the senses may be hyper-acute and the brain
lacks the ability to prioritise some sensory information
over others (Miller 2006). This affects the way in they
respond to others, in that verbal instructions compete
with a myriad of other sensory information the child is
trying to process (Miller 2006, Shandley 2012, Curtis
2010). The lack of ltering of sensory information,
combined with altered connectivity within the brain,
slows processing time and results in delayed or absent
responses from the child.
Children on the spectrum express SPD in a few
different ways. Some are described as exhibiting
sensory-seeking behaviour, sensory under-responsivity,
and sensory overload or defensiveness. When a child
exhibits sensory-seeking behaviour, they seek activities
that exhilarate the senses in order to control sensory
input and maintain a sense of equilibrium, for example
running, jumping or spinning (Curtis 2010).
Children who exhibit sensory under-responsivity
tend more to withdraw, or seek quiet, sedentary games,
or have reclusive interests. These children may also be
unresponsive to their own physical needs (eg: toilet,
hunger, food left on face, runny nose). They may be slow
or unmotivated to learn to dress themselves, slow with
toilet training, unresponsive to changes in temperature
and unaware of what is going on around them. Children
Table 4: Common co-morbidities in children with ASD
Condition Prevalence Reference
Anxiety < 84% Davis 2011, White 2009
Sleep disorders 75% Teirney 2004
Allergic manifestations
(asthma, atopic dermatitis and/or
allergic rhinitis)
52% Mostafaa 2008
Depression < 50% Teirney 2004
ADHD 45% of children with ASD meet the
diagnostic criteria for ADHD
Skokauskas 2012
Symptoms of epilepsy 33% Teirney 2004
Obsessive-compulsive disorder 10% Gjevik 2010
Tourette’s syndrome 6% Teirney 2004
Fragile X Syndrome 1% Teirney 2004
Australian Journal of Herbal Medicine 2013 25(3)
133© National Herbalists Association of Australia 2013
with SPD may also exhibit characteristics of both sensory
under-responsivity and sensory seeking at different times
(Miller 2006).
Sensory overload/defensiveness occurs when the
individual who is unable to lter out background sensation
(smell, sight, sound, touch, taste, proprioception) becomes
overwhelmed (Miller 2006, Shandley 2012). Sensory
overload creates enormous anxiety for the individual
and the person will often try to “escape” a challenging/
overwhelming situation (Miller 2006, Curtis 2010). A
person may use appropriate or inappropriate means to
remove themselves or withdraw from a situation. When
anxiety levels are high, ght or ight mechanisms are
used and the ability of the individual to think clearly and
make appropriate decisions is diminished (Curtis 2010).
Level of skill, or ability to make situation appropriate
choices reduces in proportion to the increase in level of
anxiety being experienced (Curtis 2010). Disruptive or
challenging behaviours are often used by children with
SPD in situations where they feel overwhelmed because
they lack the skills to gure out how to withdraw from a
challenging situation in a way that is socially appropriate.
The unfortunate outcome of these situations is often
discipline, punishment, further alienation and lowered
self-esteem (Curtis 2010).
Occupational therapy may be used to help the child
learn appropriate means to remove themselves from a
situation when feeling overwhelmed. However it is equally
important that carers and teachers are aware of the child’s
individual triggers. Observation in the classroom by the
occupational therapist helps with this process, followed by
negotiation involving teacher, parent, therapist and child
to make the class-room a less overwhelming environment
and more conducive to the child’s learning (Curtis 2010).
Fundamental to this process are agreed-upon means by
which the child can withdraw to a quiet space or engage
in physical activity when needed.
Mortality rates have been found to be at least double
the rate of the neurotypical population, with one study
suggesting it is 5.6 times the expected rate (Gillberg 2010,
Mouridsen 2008). This rate was higher in females than
males (Gillberg 2010). Seizures are a large contributor to
mortality rates. Impulsivity and compulsivity may also
be signicant contributing factors. Parents of children on
the spectrum are often hyper-vigilant with their children
because they are aware that their child is compulsive and
additionally may not be able to predict cause and effect.
Multidisciplinary management of autism
Autism requires a multidisciplinary approach and
will need good communication between therapists. For
practicality, parents will often have to prioritise some
therapies over others, depending on the child’s specic
needs at the time (Table 5).
Evidence-based natural therapies and
lifestyle recommendations
Many strategies the natural therapist may employ will
be based on assessing the individual needs of the patient
alongside an understanding of what we now know to be
the underlying pathophysiology of autism. While much
of this research is preliminary, the following treatments
have an evidence base.
Gluten free casein free diet (GFCF)
A controlled, single-blind, Scandinavian trial in 2010
found improvements in core autistic behaviours using
a gluten-free casein-free diet (GFCF diet) over an 8-12
month period (Whitely 2010). This study found a higher
dropout rate with adolescent patients. Improvements
were observed in communication, social functioning,
attention, concentration and hyperactivity. Improvements
in social interactiveness, and stereotyped and repetitive
behaviours were observed after 24 months (Whiteley
2010). A pilot study in 2012 noted that whilst 100% of
parents with a child on a GFCF diet noticed improvements
in behaviour and gastrointestinal symptoms, these results
were not clinically veriable (Harris 2012). It is important
Table 5: Medical and allied health professionals involved in the care of children with ASD
Therapist Role
Paediatrician Initial diagnosis;
access to funding/rebates;
Co-ordinate and prioritise therapies.
Speech therapist Assist with language delays, stutter, disorganised speech, and orosensory motor issues
Address sensory overload/defensiveness issues;
negotiates with school to adapt classroom and develop routines to accommodate child’s needs;
Facilitates social development; may help with fine motor skills.
Physiotherapist Assists with developing gross motor skills.
Psychologist Assist with developing social skills as well as specific issues such as sibling rivalry, bullying, victimising,
exclusion, and poor self-esteem.
Psychiatrist More often involved with the older child or adult.
Psychotropic medication use has been reported as 45% of children and adolescents with autism (Golink 2010).
Australian Journal of Herbal Medicine 2013 25(3)
134 © National Herbalists Association of Australia 2013
to note that this study used a reduced gluten and casein
diet (8.7 gluten or casein foods per week, compared to 53
for the control) rather than a strict GFDF diet.
These results were not seen in a 2011 study over a
three month period (Johnson 2011). Possible limiting
factors were the difculty of not being able to blind
parents to the treatment regime and that the control used
was a healthy low-sugar diet.
Fundamental to the success or failure of a gluten-free
diet is the capacity to provide appropriate food substitutes
for gluten-containing foods. Other issues that may limit
success may include the willingness of parents to adapt
to a new diet and the willingness of the child to try new
foods. Other factors such as oro-sensory issues, other
food allergies or intolerances and a history of previous
attempts at dietary exclusions may also be a limitation.
To assess these issues a 2008 pilot study focused
on developing an acceptable protocol and method for
assessing a GFCF diet (Adams 2008). The authors of this
study attempted to develop a range of foods that children
would accept and that were transportable, easy to prepare
and nutritionally suitable. Given the habitual tendencies
and food fussiness inherent in many children with ASD,
the trial aimed to assess the willingness of children to
try new foods. Recruitment consisted of 52 children aged
3-6 years. The study found that 95% of the children tried
some of the new foods and only three families dropped
out of the study due to food refusal. Parents commented
that there needed be a savoury staple (e.g. bread)
included. The authors concluded that families of these
children were very motivated to participate in dietary
research specic to ASD and that nding acceptable
food substitutes is critical for this kind of study to be of
clinical signicance (Adams 2008).
Vitamin C
A 30 week double-blind placebo-controlled trial
showed decreased symptom severity in children with
ASD. A dose of 8g/70kg/day of ascorbic acid resulted
in signicant improvement in total interaction scores
and sensory motor scores. The mechanism of action
may be via the dopamine-potentiating effect of vitamin
C demonstrated in earlier studies, in addition to its
antioxidant role (Dolske 1993, Shin 1988).
Multivitamin-mineral supplement
A small pilot study of 20 children aged 3-8 years with
ASD investigated the effects of a “moderate” multivitamin
supplement. The study reported signicant improvements
in gastrointestinal symptoms and sleep (Adams 2004).
Vitamin B6
Vitamin B6 is a co-factor for 113 enzymes,
including neurotransmitters serotonin, GABA and the
catecholamines (Adams 2006). Supplementation of
vitamin B6 in ASD has been extensively studied. Of 22
studies conducted, 21 show improvement in ASD (Bihari
2006). Pyridoxal kinase has been demonstrated to have
very low activity in children with autism (Adams 2006).
Low activity of pyridoxal kinase results in low levels
of pyridoxal-5-phosphate (PLP) and high plasma levels
of total B6, due to impaired conversion of pyridoxine
and pyridoxal to PLP (Adams 2006). Plasma levels of
total B6 have been observed to be 75% higher in autistic
children (Meletis 2007).
High dose B6 may improve function of pyridoxal
kinase, which may explain improvements in mental and
physical function in ASD (Adams 2006). Doses used in
studies ranged 100-600mg/day (Pfeifferi 1995).
Magnesium and B6
Red-blood-cell levels of magnesium have been observed
to be lower in children with ASD (Meletis 2007). In 2006
a study was conducted using magnesium (6mg/kg/d) and
B6 (0.6mg/kg/d) in autistic children. Seventy percent of
children showed signicant improvement (Meletis 2007).
Additionally there is positive research to support the use
magnesium in the treatment of anxiety (Lakhan 2010). It
is therefore well worth considering in patients with ASD.
Vitamin B12 and Folic Acid
People with ASD have reduced methylation of
S-adenosylmethionine (SAM) to S-adenosylhomocysteine
(SAH), and Glutathione (GSH) to its oxidised form
Glutathione disuphide (GSSG). These ratios (SAM:SAH)
and (GSH:GSSG) are indicative of reduced methylation
capacity and increased oxidative stress. A 2009 study used
75mcg/kg injected methylcobalamine with 400mg folinic
acid daily for 3 months. This resulted in improved serum
ratios but not normalised to levels of neurotypical people.
Despite this, signicant improvements in behavioural
symptoms were observed. This nding is consistent with
other studies (James 2009, Bertoglio 2010).
An eight week trial (n=31) using 800mg L-carnosine
showed signicant improvement in behaviour,
communication and social ASD traits (Chez 2002). Mild
improvements in other ASD traits were also observed.
Carnosine is an antioxidant, has antiglycating activity
and binds heavy metals (Meletis 2007). Carnosine also
appears to enhance frontal lobe function, and have a
neuroprotective effect (Chez 2002).
Omega 3 fats
The need for adequate levels of EPA and DHA is seen
especially during pregnancy. However, strategies that
utilise neuroplasticity could also benet from the uidity
provided by these nutrients. Neuroplasticity requires
cell uidity to develop new axons, dendritic extensions
and synapses, and DHA is the most uid component of
cell membranes (Kidd 2007). Many studies have been
conducted to assess the clinical application of omega 3
fats in the treatment of autism.
Australian Journal of Herbal Medicine 2013 25(3)
135© National Herbalists Association of Australia 2013
In 2007 a small 6-week pilot study (DBPC n=12) was
conducted in boys with ASD aged 5-17 years (Amminger
2007). Test subjects were given 7g sh oil (FO) in
capsules (840mg EPA, 700 mg DHA, 7mg vitamin E).
Placebo consisted of 1g Coconut oil, 1mg vitamin E,
1mg FO to mimic shy taste. The results of this study
demonstrated a mild improvement in inappropriate
speech (39%), and larger improvements with stereotypy
(72%) and hyperactivity (71%) (Amminger 2007).
In 2009 a systematic review was conducted in which
only 6 out of the retrieved 143 studies satised the inclusion
criteria and were included (Bent 2009). The authors reported
that while there is broad use of FO supplementation in
ASD, so far there is little quality evidence to support it
(Bent 2009). Similarly a 2011 Cochrane review concluded
insufcient statistical evidence (James 2011). Inherent
difculties in adequately assessing evidence for the use
of omega 3 fats in ASD include the inability to easily
blind a benign placebo, the use of inadequate doses, and
recruitment of small sample sizes.
A 2012 meta-analysis concluded that exercise
signicantly improves motor skills, social skills and
communication skills (Sowa 2012). Most studies
consisted of small groups and lacked a control group.
Most studies achieved a positive result in the targeted
area. Exercise regimes included cycling, aerobic exercise,
swimming and horse riding (Table 6).
A 2011 Cochrane review included 10 trials that
involved 390 children with ASD. Age ranged from
3-18 years and the treatment duration ranged from
four weeks to nine months (Cheuk 2011). The authors
concluded that there is no statistical evidence to support
the use of acupuncture in children with ASD. However,
2 trials showed improvement in secondary outcomes of
communication, linguistic ability, cognitive function and
global functioning. A further 6 trials showed improvement
in secondary outcomes of cognitive function and global
functioning. A positive result was also found in secondary
outcomes in 2 acupressure trials, which showed
improvement in communication and linguistic ability,
cognitive function and global functioning (Cheuk 2011).
Interpretation of reviews is limited by target outcomes,
the quality of original studies and the qualitative nature of
assessing core ASD features. While these studies did not
show improvement in target areas, they did demonstrate
improvement in other areas of difculty in ASD and as
such may be clinically relevant.
Animal assisted therapy
Animals may play a role in improving the quality of
life of children and adults with autism. In severe cases
this may be as a service dog (Adams 2010). In most cases,
however, this is more likely to be the household pet. The
child may be given set tasks involved with the care of
the animal, so that they develop a sense of responsibility.
Having a pet helps a child develop empathy, consideration
of others’ feelings and self-condence (Adams 2010, Law
1995). The animal may also be a source of comfort and
unconditional love for the child. Prosocial behaviours
such as offering to share and offering comfort, has also
been observed in autistic children with the introduction
of a pet (Grandgeorge 2012). Care must be taken when
making this recommendation. People on the spectrum
often are atopic, may have specic phobias, and their
families are often extraordinarily busy. It is important to
consider the type of pet and the potential negative and
positive outcomes for the child and their family within
the scope of this recommendation.
Autism is a very complex condition that requires
a multidisciplinary approach to maximise the child’s
potential. It is important to have a thorough understanding
of the pathophysiology underlying this complex disorder
in order to understand the core characteristics present in
autistic children. Research developments have improved
the understanding of the aetiology and pathophysiology of
autism spectrum disorders, which can now be considered
Table 6: Effect of exercise on ASD symptoms
Exercise Study size Outcome Reference
Cycling n=3 Improvements in terms of self-efficacy, group participation and physical
Todd 2010
Aerobic exercise n=5 Reduction in self-stimulatory behaviour. Participants performed better
at set tasks, both in terms of accuracy and amount of tasks completed.
Swimming n=16 Increased water confidence and competence. Decreased antisocial
behaviour, but not increased social competence.
Valuable opportunity for peer support, socialising and verbal instruction
Pan 2010
Horse riding n=29 Improved self-concept. Cawley 1994
Horse riding n=19 Improved sensory receptivity and social motivation.
Less sedentary behaviours and distractibility.
Bass 2009
Australian Journal of Herbal Medicine 2013 25(3)
136 © National Herbalists Association of Australia 2013
to be genetic, neurological, immunological, pro-
inammatory and pro-oxidant. While there is preliminary
research of some natural therapies and dietary approaches,
there is great scope for further research as to the role of
complementary therapies in the treatment of autism.
These therapies range from lifestyle and exercise regimes,
to nutritional supplementation and dietary modication.
Further research as to how complementary therapies might
be used to maximise the potential of children with autism
and support other modalities is therefore warranted.
Adams JB, George F, Audhya T. 2006. Abnormally High Plasma Levels
of Vitamin B6 in Children with Autism Not Taking Supplements
Compared to Controls Not Taking Supplements. J Altern
Complement Med 12:1;59–63.
Adams JB, Holloway CA. 2004. Pilot study of a moderate dose
multivitamin/mineral supplement for children with autistic spectrum
disorder.r J Altern Complement Med 10:6;1033-1039.
Adams N. 2010. Review of Animal-assisted interventions for
individuals with autism. J. Autism Dev. Disord 40:1;132-133.
Adams SJ, Burton N, Cutress A, Adamson AJ, McColl E, O’Hare A,
Baird G, Le Couteur A. 2008. Development of double blind gluten
and casein free test foods for use in an autism dietary trial. The
British Dietetic Association Ltd. J Hum Nutr Diet 21;373–406.
Agam Y, Joseph RM, Barton JS, Manoach DS. 2010. Reduced cognitive
control of response inhibition by the anterior cingulate cortex in
autism spectrum disorders. Neuroimage 52:1;336-347.
Aldred S, Moore KM, Fitzgerald M, Waring RH. 2003. Plasma Amino
Acid Levels in Children with Autism and Their Families. J. Autism
Dev. Disord 33:1;93-97.
Al-Farsi YM, Al-Sharbati MM, Waly MI, Al-Farsi OA, Al-Shafaee
MA, Al-Khaduri MM, Trivedi MS, Deth RC. 2012. Effect of
suboptimal breast-feeding on occurrence of autism: A case–control
study. Nutrition 28;e27–e32.
Amminger GP, Berger GE, Schäfer M, Klier C, Frierich MH, Feucht M.
2007. Omega-3 fatty acids supplementation in children with autism:
A double-blind randomized, placebo-controlled pilot study. Biol
Psychiatry 61:4;551-553.
Baeza-Velasco C, Michelon C, Rattaz C, Pernon E, Baghdadli A.
2013. Separation of Parents Raising Children with Autism Spectrum
Disorders. J Dev Phys Disabil DOI 10.1007/s10882-013-9338-0.
Bass MM, Duchowny CA, Llabre MM. 2009. The effect of therapeutic
horseback riding on social functioning in children with autism. J.
Autism Dev. Disord 39;1261–1267.
Bent S, Bertoglio K,. Hendren RL. 2009. Omega-3 Fatty Acids for
Autistic Spectrum Disorder: A Systematic Review. J Autism Dev
Disord 39;1145–1154.
Bertoglio K, James J, Deprey L, Brule N, Hendren RL. 2010. Pilot
Study of the Effect of Methyl B12 Treatment on Behavioral and
Biomarker Measures in Children with Autism. J Altern Complement
Med 16:5;555–560.
Bihari T. 2006. Assessing CAM Options for Treating Autism.
Alternative and Complementary Therapies 12:5;233.
Cawley R; Cawley D; Retter K. 1994. Therapeutic Horseback Riding
and Self-Concept in Adolescents with Special Educational Needs.
Anthrozoos: A Multidisciplinary Journal of The Interactions of
People and Animals 7:2;129-134.
Cheuk DKL, Wong V, Chen WX. 2011. Acupuncture for autism
spectrum disorders (ASD) (Review) The Cochrane Collaboration.
Published by JohnWiley and Sons, Ltd.
Chez M, Buchanan CP, Aimonovitch MC, Becker M, Schaefer K,
Black C, Komen J. 2002. Double-Blind, Placebo-Controlled Study
of L-Carnosine Supplementation in Children With Autistic Spectrum
Disorders Michael G. Chez, Journal of Child Neurology 17:11;833-
Constantino JN, Zhang Y, Frazier T, Abbacchi AM, Law P. 2010.
Sibling recurrence and the genetic epidemiology of autism. Am J
Psychiatry 167:1349–1356.
Croen LA, Grether JK, Yoshida CK, Odouli R, Hendrick V. 2011.
Antidepressant Use During Pregnancy and Childhood Autism
Spectrum Disorders. Arch Gen Psychiatry 68:11;1104-1112.
Croen LA, Najjar DV, Fireman B, Grether JK. 2007. Maternal and
paternal age and risk of autism spectrum disorders. Arch Pediatr
Adolesc Med:161:334–340.
Curtis T. 2010. FABIC Touring Conference (Positive Behavioural
Interventions for People Using Challenging Behaviours). Hobart
Sept 2010.
Davis TE, Moree BN, Dempsey T, Reuther ET, Fodstad JC, Hess
JA, Jenkins WS, Matson JL. 2011. The relationship between
autism spectrum disorders and anxiety: The moderating effect of
communication. Research in Autism Spectrum Disorders 5;324–329.
Dolske MC, Spollen J, McKay S, Lancashire E, Tolbert L. 1993. A
preliminary trial of ascorbic acid as supplemental therapy for autism.
Prog Neuropsychopharmacol Biol Psychiat 17;765–774.
Entiticotti PG, Rinehart NJ, Tonge BJ, Bradshaw JL, Fitzgerald PB.
2010. A preliminary transcranial magnetic stimulation study of
cortical inhibition and excitability in high-functioning autism and
Asperger disorder. Developmental Medicine and Child Neurology
Fatemi SH, Reutiman TJ, Folsom TD, Rooney RL, Patel DH, Thuras
PD. 2010. mRNA and Protein Levels for GABAAa4, a5, b1 and
GABABR1 Receptors are Altered in Brains from Subjects with
Autism. J Autism Dev Disord 40:743–750.
Fatemi SH, Reutiman TJ. Folsom TD, Thuras PD. 2009. GABA(A)
Receptor Downregulation in Brains of Subjects with Autism. J
Autism Dev Disord 39;223–230.
Fernell E. 2010. Serum levels of 25-hydroxyvitamin D in mothers of
Swedish and of Somali origin who have children with and without
autism Acta Pædiatrica 99;743–747.
Gardener H, Spiegelman D, Buka SL. 2009. Prenatal risk factors
for autism: comprehensive meta-analysis. The British Journal of
Psychiatry 195:7–14.
Gillberg C, Billstedt E, Sundh V, Gillberg IC. 2010. Mortality in
autism: a prospective longitudinal community-based study. J Autism
Dev Disord 40:3;352-7
Gjevik E, Eldevik S, Fjæran-Granum T, Sponheim E. 2010. Kiddie-
SADS Reveals High Rates of DSM-IV Disorders in Children and
Adolescents with Autism Spectrum Disorders. Journal of Autism and
Developmental Disorders: Published online: http://link.springer.
Golink A, Maccabee-Ryanboy N. 2010. Autism: Clinical Pearls
for Primary Care. Contemporary Paediatrics 42-60. http://
Grandgeorge M, Hausberger M, Tordjman S, Lazartigues A, Lemonnier
E, Deleau M. 2012. Does Pet Arrival Trigger Prosocial Behaviors in
Individuals with Autism? PLoS ONE 7:8;e41739.
Harris C, Card B. 2012. A pilot study to evaluate nutritional inuences
on gastrointestinal symptoms and behavior patterns in children with
Autism Spectrum Disorder. Complementary Therapies in Medicine
Hartley SL, Barker ET, Mailick Seltzer M, Greenberg JS, Floyd FJ.
2011. Marital satisfaction and parenting experiences of mothers and
fathers of adolescents and adults with autism spectrum disorders.
American Journal of Intellectual and Developmental Disabilities
Higgins DJ, Bailey SR, Pearce JC. 2005. Factors associated with
functioning style and coping strategies of families with a child with
an autism spectrum disorder. Autism 9;125-137.
James S, Montgomery P, Williams K. 2011. Omega-3 fatty acids
supplementation for autism spectrum disorders (ASD). The
Cochrane Collaboration. Published by John Wiley and Sons, Ltd.
James SJ, Melnyk S, Fuchs G, Reid T, Jernigan S, Pavliv O, Hubanks
Australian Journal of Herbal Medicine 2013 25(3)
137© National Herbalists Association of Australia 2013
A, and Gaylor DW. 2009. Efcacy of methylcobalamin and folinic
acid treatment on glutathione redox status in children with autism.
Am J Clin Nutr 89;425–30.
Johnson CR, Handen BL, Zimmer M, Sacco K, Turner K. 2011. Effects
of Gluten Free / Casein Free Diet in Young Children with Autism: A
Pilot Study. J Dev Phys Disabil 23;213–225
Juul-Dam N, Townsend J, Courchesne E. 2001. Prenatal, Perinatal,
and Neonatal Factors in Autism, Pervasive Developmental Disorder
- Not Otherwise Specied, and the General Population. Pediatrics
Kaufmann WE. DSM-V: The New Diagnostic Criteria for Autism
Spectrum Disorders. Department of Neurology Boston Children’s
Hospital, Harvard Medical School.
Kenet T, Orekhova EV, Bharadwaj H, Shetty NR, Israeli E, Lee AK,
Agam Y, Joseph RM, Hinen MS, Manoach DS. 2012. Disconnectivity
of the cortical ocular motor control network in autism spectrum
disorders. Neuroimage [Epub ahead of print] 11 Mar 2012.
Kidd PM. 2003. An Approach to the Nutritional Management of
Autism. Alternate Therapies 9:5;22-31.
Kidd PM. 2007. Omega 3 DHA and EPA for Cognition, Behavior, and
Mood: Clinical Findings and Structural-Functional Synergies with
Cell Membrane Phospholipids. Altern Med Rev 12:3;207-227.
Kushak R, Lauwers G, Winter S, Buie T. 2011. Intestinal disaccharidase
activity in patients with autism. Autism SAGE Publications and The
National Autistic Society 15:3;285–294.
Lakhan SE, Vieira KF. 2010. Nutritional and herbal supplements for
anxiety and anxiety-related disorders: systematic review. Nutr J
Law S, Scott S. 1995. Pet care: A vehicle for learning. Focus on Autistic
Behavior 10:2;17.
Lofholm N. 2008. Autism’s terrible toll: Parents risk hitting “a breaking
point.” Denver Post 12/02/2008
London E. 2007. The role of the neurobiologist in redening the
diagnosis of autism. Brain Pathol 17:4;408-411.
Mailick Seltzer M, Floyd FJ, Song J, Greenberg JS, Hong J. 2011.
Midlife and Aging Parents of Adults with Intellectual and
Developmental Disabilities: Impacts of Lifelong Parenting. Am J
Intellect Dev Disabil. 116:6;479–499.
Matson JL, Fodstad, JC, Dempsey T. 2009. What symptoms predict
the diagnosis of autism or PDD-NOS in infants and toddlers with
developmental delays using the Baby and Infant Screen for AutIsm
Traits. Developmental Neurorehabilitation 12:6;381–388
McGinnis WR. 2004. Oxidative Stress in Autism. Alternative Therapies
Mefford HC, Batshaw ML, and Hoffman EP. 2012. Genomics,
Intellectual Disability, and Autism. N Engl J Med 366;8.
Meguid NA, Atta HM, Gouda AS, Khalil RO. 2008. Role of
polyunsaturated fatty acids in the management of Egyptian children
with autism. Clinical Biochemistry 41:1044–1048.
Meguid NA, Hashish AF, Anwar M, Sidhom G. 2010. Reduced
Serum Levels of 25-Hydroxy and 1,25-Dihydroxy Vitamin D in
Egyptian Children with Autism. The Journal of Alternative and
Complementary Medicine 16:6; 641–645.
Meletis CD, Zabriskie N. 2007. Is Autism the Coal Miner’s Canary
of America’s Health Status? Alternative and Complementary
Therapies: August. 13:4;193-198.
Miller LJ. 2006. Sensational Kids: Hope and Help for Children with
Sensory Processing Disorder, 1st Edition, New York, Penguin Group.
Mostafa GA, El-Sherif DF, Hamza RT, Al Shehab A. 2008.
Hyperserotonemia in Egyptian autistic children: Relation to allergic
manifestations. Journal of Pediatric Neurology 6:3;227-236.
Mostafaa GA, Hamzaa RT and. El-Shahawib HH. 2008. Allergic
manifestations in autistic children: Relation to disease severity.
Journal of Pediatric Neurology 6:3; 227-236.
Mouridsen SE, Bronnum-Hansen H, Rich B, Isager T. 2008. Mortality
and causes of death in autism spectrum disorders: an update. Autism
Mundkur, N. 2005. Neuroplacticity in Children. Indian Journal of
Paediatrics 72;855-857.
Naseef R, Freedman B. 2012. A Diagnosis of Autism is not a Prognosis
of Divorce. Myths and Realities of Maintaining a Marriage as
Parents of a Child with Autism. Autism Advocate: Fall:8-12.
Pan CY. 2010. Effects of water exercise swimming program on
aquatic skills and social behaviors in children with autism spectrum
disorders. Autism 14:1;9–28.
Patterson PH. 2009. Immune involvement in schizophrenia and autism:
Etiology, pathology and animal models. Behavioural Brain Research
Patterson PH. 2011. Maternal infection and immune involvement in
autism. Trends in Molecular Medicine 17: 7;398-394.
Pfeifferi SI, Norton J, Nelson L, Shott S. 1995. Efcacy of Vitamin B6
and Magnesium in the Treatment of Autism: A Methodology Review
and Summary of Outcomes. Journal of Autism and Developmental
Disorders 25:5;481-493.
Politi P, Cena H, Comelli M, Marrone G, Allegri C, Emanuele E,
Ucelli di Nemi S. (2008). Behavioral effects of omega-3 fatty acid
supplementation in young adults with severe autism: An open label
study. Archives of Medical Research 39:682–685.
Rosenthal-Malek A, Mitchell S. 1997. Brief Report: The Effects of
Exercise on the Self-Stimulatory Behaviors and Positive Responding
of Adolescents with Autism. Journal of Autism and Developmental
Disorders 27: 2; 193-202
Samtani A, Sterling-Levis K, Scholten R, Woolfenden S, Hooft L,
Williams K. 2011. Diagnostic tests for Autism Spectrum Disorders
(ASD) in preschool children. The Cochrane Collaboration.
Published by JohnWiley and Sons, Ltd.
Shandley K, Austin DW. 2012. Reconceptualizing Autism: Moving
Beyond the Behavioral to Address Cause, Cure and Prevention.
Autism Insights 2010:2.
Shin SH, Stirling R. 1988. Ascorbic acid potentiates the inhibitory
effect of dopamine on prolactin release in primary cultured rat
pituitary cells. J. Endocr: 118:287–294.
Skokauskas N, Gallagher L. 2012. Mental health aspects of autistic
spectrum disorders in children. Journal of Intellectual Disability
Research 56:3;248-57.
Smith SEP, Li J, Garbett, J, Mirnics K, Patterson PH. 2007. Maternal
Immune Activation Alters Fetal Brain Development through
Interleukin-6. J Neurosci. 27:40;10695–10702.
Sowa M, Meulenbroek R. 2012. Effects of physical exercise on Autism
Spectrum Disorders: A meta-analysis. Research in Autism Spectrum
Disorders 6;46–57.
Takahata K, Kato M. 2008. Neural mechanism underlying autistic
savant and acquired savant syndrome. Brain Nerve 60:7;861-9.
Teirney E. 2004. Co-Morbidity in Autism. The Exceptional Parent:
Todd T. 2010. Cycling for Students With ASD: Self-Regulation
Promotes Sustained Physical Activity. Adapted Physical Activity
Quarterly 27:226-241.
Tomeny TS, Barry TD, Bader SH. 2012. Birth order rank as a moderator
of the relation between behavior problems among children with
an autism spectrum disorder and their siblings. Autism DOI:
Vaccarino FM, Grigorenko EL, Mueller Smith K, Stevens HE. 2009.
Regulation of Cerebral Cortical Size and Neuron Number by
Fibroblast Growth Factors: Implications for Autism. J Autism Dev
Disord 39;511–520.
Wagner GC, Reuhl KR, Cheh M, McRae P, Halladay AK. 2006. New
Neurobehavioral Model of Autism in Mice: Pre- and Postnatal
Exposure to Sodium Valproate. J Autism Dev Disord 36;779–793
White SW, Oswald D, Ollendick T, Scahill L. 2009. Anxiety in children
and adolescents with autism spectrum disorders. Clinical Psychology
Review 29;216–229.
continued on page 151
Australian Journal of Herbal Medicine 2013 25(3)
151© National Herbalists Association of Australia 2013
include direct antibacterial activity, indirect antibacterial
activity such as inhibition of host epithelia and group A
streptococci, improved phagocytosis, improved oxidative
burst and intracellular killing by human peripheral blood
phagocytes, release of tumour necrosis factor and nitric
oxides and a number of other activities. Previous meta-
analysis of clinical trials with EPs 7630 in acute bronchitis
indicate superior efcacy in symptom resolution when
compared with placebo. The current study was the rst
to extend this research to COPD patients and examine
whether EPs 7630 administration could reduce time to
rst exacerbation and reduce exacerbation frequency as
an adjunctive therapy.
The randomised, double-blind, placebo-controlled
trial involved 200 patients with chronic bronchitis from
18 centres across the Ukraine. Over a 24-week treatment
period the participants took either EPs 7630 or matched
placebo as an add-in treatment to their existing regime.
Dosing of the medication was 3 x 30 drops daily. Over
the course of the study participants documented on a
daily basis: chronic bronchitis symptoms, health status
and consumption of all medications. In addition they
undertook seven regular visits to the treatment centre and
intermediary visits in case of an exacerbation. Baseline
assessments included: physical examinations, laboratory
tests, chest X-ray, bronchitis symptom score of cough,
sputum and sternal chest pain, and spirometry tests to
determine FEV1 and FVC before and after ipratropium-
bromide/fenoterol (NB. this was used in the place of
salbutamol in reversibility testing as salbutamol was not
available in the Ukraine at this time).
The primary outcome measure of the study was time
to rst COPD exacerbation (reported or unreported, as
assessed by increases in medication to self-manage
COPD symptomatology). Secondary outcome measures
were: number and duration of exacerbations, health
status, patient satisfaction with treatment and duration of
inability to work.
Overall median time to exacerbation was 57 days in
the EPs 7630 group and 43 days in the placebo group. The
probability of remaining free of COPD exacerbation was
signicantly higher in the active treatment group. For EPs
7630 patients the median duration of exacerbation was
also a day shorter (11 v 12 days) and far fewer required
antibiotic treatment (37.8% of patients compared with
73.3% of patients on placebo). Patient satisfaction with
the intervention was signicantly higher in the active
treatment group after 24 weeks and the mean number of
days off work was also signicantly lower in this group.
However the rates of mild gastrointestinal disturbance
were higher in the Pelargonium treatment arm.
The results of this study indicate that EPs 7630 (and
by extrapolation, similar extracts of Pelargonium) may
be of use as an additional treatment to prevent and treat
exacerbations in patients with moderate to severe chronic
Anti-aging effects of Withania Somnifera
Kumar R, Gupta K, Saharia K, Pradhan D, Subramaniam J. 2103.
Withania somnifera root extract extends lifespan of Caenorhabditis
elegans. Ann of Neurosc DOI:0.5214/ans.0972.7531.200106.
Withania Somnifera (WS) is a herb most Western
herbalists are familiar with. It has a long history of use
in Ayurvedic medicine, in which it is claimed to have
longevity-enhancing effects. However this has never
been proven.
Researchers from the Indian Institute of Technology in
Kanpur set out to evaluate whether an extract of Withania
Somnifera root could indeed have anti-ageing effects.
In the past the major challenge with studies assessing
lifespan was the long-time requirement in mammalian
models (even murine models). However recent studies
now use the model organism Caenorhabditis elegans,
an organism with fundamental mechanisms and systems
similar to the mammalian system. This organism has
a naturally short lifespan but the mechanisms which
increase its longevity, identied in previous studies of C.
elegans, are remarkably similar to those reported in mice,
ies and humans.
They found that when C. elegans worms were treated
with WS extracts, they demonstrated a 21.4% lifespan
extension in comparison to control. This research must
be taken with a grain of salt as it was funded by the
company that produced the extract and it is only initial
data. However it opens interesting avenues for further
investigation. Herbalists may wish to consider WS as
part of a healthy-ageing strategy for those clients who
wish to optimise their health as they age.
Whiteley P, Todd L, Dodou K and Shattock P. 2009. Trends in
Developmental, Behavioral and Somatic Factors by Diagnostic Sub-
group in Pervasive Developmental Disorders: A Follow-up Analysis.
Autism Insights 2009:1
Whiteley, P, Haracopos D, Knivsberg A, Ludvig Reichelt K, Parlar S,
Jacobsen J, Seim A, Pedersen L, Schondel M, Shattock. P. 2010. The
ScanBrit randomised, controlled, singleblind study of a gluten- and
casein-free dietary intervention for children with autism spectrum
disorders. Nutritional Neuroscience 2010:13:2; 87.
Winfrey O 2007. The Oprah Winfrey show the faces of autism. April 05,
Woodbury-Smith MR, Volkmar FR. 2009. Asperger syndrome.
European Child and Adolescent Psychiatry 18:1
Zimmerman AW, Connors SL, Matteson KJ, Lee L, Singer HS,
Castaneda JA, Pearce DA. 2007. Maternal antibrain antibodies in
autism. Brain, Behavior, and Immunity 21;351–357.
Autism spectrum disorder: A review of the current understanding of pathophysiology and
complementary therapies in children References continued from page 137
Reproduced with permission of the copyright owner. Further reproduction prohibited without
... Pada tahun 2002 tingkat autisme dilaporkan 6,6 banding 1000 dan terus meningkat menjadi 15-20 banding 1000 pada tahun 2013. 3 Gangguan ini juga cenderung meningkat setiap tahunnya di Indonesia, menurut World Health Organization (WHO) pada tahun 2013 terjadi peningkatan prevalensi di Indonesia dalam sepuluh tahun terakhir yaitu dari satu per 1000 penduduk menjadi delapan per 1000 penduduk. 3 Provinsi Jawa Barat juga mengalami kecenderungan peningkatan jumlah anak GSA setiap tahunnya yakni mencapai 1.085 anak pada tahun 2011 dan di Kota Bandung pada tahun 2007 mencapai 739 orang atau sekitar sepuluh persen dari penderita gangguan ini di Indonesia. ...
... 3 Gangguan ini juga cenderung meningkat setiap tahunnya di Indonesia, menurut World Health Organization (WHO) pada tahun 2013 terjadi peningkatan prevalensi di Indonesia dalam sepuluh tahun terakhir yaitu dari satu per 1000 penduduk menjadi delapan per 1000 penduduk. 3 Provinsi Jawa Barat juga mengalami kecenderungan peningkatan jumlah anak GSA setiap tahunnya yakni mencapai 1.085 anak pada tahun 2011 dan di Kota Bandung pada tahun 2007 mencapai 739 orang atau sekitar sepuluh persen dari penderita gangguan ini di Indonesia. 5 Anak dengan GSA seringkali mengalami kendala dalam memelihara ataupun meningkatkan kesehatan gigi dan mulut. ...
... Hal ini yang kemudian menimbulkan reaksi mekanisme fight or flight sehingga anak berusaha untuk menolak atau menarik diri dari situasi yang dianggap menakutkan tadi. 3 Reaksi fight or flight merupakan reaksi fisiologis dan respon tubuh yang terjadi secara otomatis terhadap stimulus yang dianggap berbahaya atau menakutkan yang membuat individu ingin melawan atau melarikan diri dari stimulus tersebut. Reaksi ini melibatkan sistem limbik pada otak tepatnya di amigdala yang berperan dalam pengendalian rasa takut. ...
Full-text available
Full-text available
The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are orthomolecular, conditionally essential nutrients that enhance quality of life and lower the risk of premature death. They function exclusively via cell membranes, in which they are anchored by phospholipid molecules. DHA is proven essential to pre- and postnatal brain development, whereas EPA seems more influential on behavior and mood. Both DHA and EPA generate neuroprotective metabolites. In double- blind, randomized, controlled trials, DHA and EPA combinations have been shown to benefit attention deficit/hyperactivity disorder (AD/HD), autism, dyspraxia, dyslexia, and aggression. For the affective disorders, meta-analyses confirm benefits in major depressive disorder (MDD) and bipolar disorder, with promising results in schizophrenia and initial benefit for borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function. Huntington disease has responded to EPA. Omega-3 phospholipid supplements that combine DHA/EPA and phospholipids into the same molecule have shown marked promise in early clinical trials. Phosphatidylserine with DHA/ EPA attached (Omega-3 PS) has been shown to alleviate AD/ HD symptoms. Krill omega-3 phospholipids, containing mostly phosphatidylcholine (PC) with DHA/EPA attached, markedly outperformed conventional fish oil DHA/EPA triglycerides in double-blind trials for premenstrual syndrome/dysmenorrhea and for normalizing blood lipid profiles. Krill omega-3 phospholipids demonstrated anti-inflammatory activity, lowering C-reactive protein (CRP) levels in a double-blind trial. Utilizing DHA and EPA together with phospholipids and membrane antioxidants to achieve a "triple cell membrane synergy" may further diversify their currently wide range of clinical applications. (Altern Med Rev 2007;12(3):207-227)
One of the most consistent biological findings in autism is elevated blood serotonin levels. Immune abnormalities, including allergy, are also commonly observed in this disorder. Allergy may play a role in pathogenesis of autism wherein immune responses to allergens may induce the production of brain autoantibodies found in many autistic children. Hyperserotonemia may be the reason behind the increased frequency of allergic manifestations in autistic children through reduction of T-helper 1-type cytokines. Thus, we investigated the possible connection between hyperserotonemia and the increased frequency of allergic manifestations in 40 autistic and 40 healthy matched children. Autistic children had significantly higher serum serotonin levels than controls [125 (250.75) vs. 41.5 (41.5) ng/mL, P < 0.001]. Fifty five percent (22/40) of autistic children had elevated serum serotonin. Allergic manifestations (bronchial asthma, atopic dermatitis and allergic rhinitis) were elicited in 45% of autistic patients which were significantly higher than controls (10%, P < 0.001). Moreover, autistic patients with allergic manifestations had significantly higher serum serotonin levels than those without (P < 0.001). Furthermore, there was a significant positive correlation between serum serotonin and total immunoglobulin E levels in autistic patients (r = 0.8, P < 0.001). In conclusion, hyperserotonemia may be a contributing factor to the increased frequency of allergic manifestations in some autistic children. Inclusion of serum serotonin levels as a correlate may be useful in future immune studies in autism to help unravel the long-standing mystery of hyperserotonemia and its possible role in the pathophysiology of this disorder. In addition, the effect of blood serotonin lowering drugs in hyperserotonemic autistic children, on amelioration of allergic manifestations and immune abnormalities, should be studied.
We examined the occurrence and timing of separation of parents raising children with Autism Spectrum Disorders followed over a 10-year period (n=119). We also compared the clinical characteristics of children and sociodemographic variables between parents who remained as a couple versus parents who separated. The results showed that after 10 years of follow-up 74.8 % of the couples remained together (n=89), representing a separation rate of 25.2 %. This rate remained stable over the study period. There was no significant difference in any of the clinical and sociodemographic variables between comparison groups. Our results suggest that raising a child with autism does not often lead to the dissolution of the parents’ relationship, as is commonly believed. The occurrence of parental separation in children with Autism Spectrum Disorders does not appear to vary according to their stage of life (childhood or adolescence). Lastly, the clinical profile of children and sociodemographic variables do not seem to influence the relationship status of parents.
Etiology of autism has become an area of significant controversy. Allergy may play a role in the pathogenesis of autism wherein allergic immune responses to some proteins (e.g., dietary proteins and latex) may induce the production of brain autoantibodies, which are found in many autistic children. This study was conducted to investigate the frequency of allergic manifestations in autistic children. The relationship between allergy and disease characteristics in terms of disease severity, clinical findings and electroencephalography (EEG) abnormalities was also studied. Fifty autistic children (30 had mild to moderate autism and 20 had severe autism) were studied in comparison to 50 age- and sex- matched children without neuropsychiatric manifestations serving as controls. Clinical evaluation was done with special emphasis on neuropsychiatric assessment and clinical manifestations of allergy. Serum total immunoglobulin E was measured in all studied subjects. In addition, EEG and assessment of mental age were done for all autistic children. Allergic manifestations (bronchial asthma, atopic dermatitis and/or allergic rhinitis) were found in 52% of autistic patients. This frequency was significantly higher than that of controls (10%; P < 0.001). There was a significant positive association between the frequency of allergic manifestations and disease severity, important clinical findings elicited in some autistic children (gastrointestinal symptoms and neurological manifestations) and EEG abnormalities. In conclusion, the frequency of allergic manifestations is increased in autistic children. The significant positive association between these manifestations and important disease characteristics (disease severity, gastrointestinal symptoms, neurological findings and EEG abnormalities) may shed light on the possible causal role of allergy in some autistic children. Indeed, we need to know more about the links between allergy, immune system and brain in autism. This is important to determine whether therapeutic modulation of immune function and allergic diseases are legitimate avenues for novel therapy in selected cases of autism or even for attempted primary prevention in genetically at risk subgroups.
It is generally agreed that regular physical exercise promotes physical and mental health, but what are the benefits in people with Autism Spectrum Disorders (ASD)? This meta-analysis evaluates 16 behavioural studies reporting on a total of 133 children and adults with various variants of the syndrome who were offered structured physical activities either in an individual or a group context. The effects on social and motor deficiencies, two of the three primary symptom clusters of ASD, were normalized to afford a quantitative evaluation. Results pertaining to communication deficits were insufficient to permit classification. All activity programmes yielded significant progress on the measures assessed, but the individual programmes elicited significantly more improvement than the group interventions in the motor and, more surprisingly, also in the social domain. Although overall sample sizes were small, the combined results do permit the tentative conclusion that in terms of motor performance and social skills children and adults with ASD benefit most from individual exercise interventions. Further research of the impact of individual and group interventions on communication deficits in particular as well as studies gauging the extent to which exercise effects depend on ASD symptom severity are warranted.
Communication skills have been shown to have differing effects on levels of anxiety depending on whether or not a child has an autism spectrum disorder (ASD) or is typically developing. This article examined whether or not communication deficits differentially affect children with ASD compared to those without ASD. Ninety-nine children with autistic disorder (n=33), Pervasive Developmental Disorder – Not Otherwise Specified (PDD-NOS; n=33), and no diagnosis (n=33) were examined using the Autism Spectrum Disorders Diagnostic for Children and Comorbidity for Children scales to determine their level of anxiety and degree of communication deficits. Results indicated that anxiety decreased as communication deficits increased for those with autistic disorder compared to those with PDD-NOS or no diagnosis; however, for those with PDD-NOS anxiety increased as communication deficits increased compared to those with no diagnosis. The importance and differential impact of communication deficits on anxiety for different groups is highlighted.