This document discusses autism spectrum disorders and potential environmental and genetic factors that may contribute to autism. It covers topics such as: - Autism is caused by genetic and environmental factors that influence early brain development. - Potential environmental factors include advanced parental age, maternal illness during pregnancy, difficult births, and combinations of genetic and environmental risks. - There is evidence that oxidative stress, issues with methylation pathways, and other biochemical abnormalities may play a role in autism. - Various studies have found associations between autism and factors like mercury exposure, inflammation, disturbances in one-carbon metabolism, and polymorphisms in genes like MTHFR.

1. By Kimmer Collison-Ris
MSN, FNP-C, WOCN, MS CAM
Images by Google
*

2. *

4. *
* Autism spectrum disorders (ASD) & autism are general terms
for a group of complex disorders of brain development.
* Believed to have its roots in early brain development yet there
is other evidence to suggest it is caused by either
* Genetics
* Faulty MTHFR genes
* post natal infections/viruses
* or environmental assaults
* These disorders are characterized, in varying degrees, by
* difficulties in social interaction,
* verbal and nonverbal communication
* repetitive behaviors.
* With the May 2013 publication of the DSM-5 diagnostic
manual, all autism disorders were merged into one umbrella
diagnosis of ASD.
* Previously, they were recognized as distinct subtypes including:
* autistic disorder,
* childhood disintegrative disorder,
* pervasive developmental disorder-not otherwise specified (PDD-
NOS)
* Asperger syndrome

5. *
*Autism statistics from the U.S.
Centers for Disease Control and
Prevention (CDC) identify around 1
in 68 American children as on the
autism spectrum–a ten-fold
increase in prevalence in 40 years.
*Careful research shows that this
increase is only partly explained
by improved diagnosis and
awareness.
*Studies demonstrate that autism is
4-5 times more common among
boys than girls.
*An estimated 1 out of 42 boys and
1 in 189 girls are diagnosed with
autism in the United States.

6. *
*There is no one cause of autism and
there is no one type of autism
*Most cases of autism appear to be
caused by a combination of
autism risk genes + environmental
factors = influence early brain
development
*RISK FACTORS:
*events before and/or during birth
or post-natally
*advanced parental age at time of
conception (both mom and dad)
*maternal illness during pregnancy
*certain difficulties during birth
(esp. fetal oxygen deprivation)
*combination of events with genetic
risk factors, appear to modestly
increase risk

7. *
* Herbert MR (2010). Contributions of the environment and environmentally vulnerable
physiology to autism spectrum disorders
* Purpose of review: This review presents a rationale and evidence for contributions of
environmental influences and environmentally vulnerable physiology to autism spectrum
disorders (ASDs). Recent findings: Recent studies suggest a substantial increase in ASD
prevalence above earlier Centers for Disease Control figures of one in 150, only partly
explicable by data artifacts, underscoring the possibility of environmental contributors
to increased prevalence. Some gene variants in ASD confer altered vulnerability to
environmental stressors and exposures. De-novo mutations and advanced parental age
as a risk factor for ASD also suggest a role for environment. Systemic and central
nervous system pathophysiology, including oxidative stress, neuroinflammation, and
mitochondrial dysfunction can be consistent with a role for environmental influence
(e.g. from air pollution, organophosphates, heavy metals) in ASD, and some of the
underlying biochemical disturbances (such as abnormalities in glutathione, a critical
antioxidant and detoxifier) can be reversed by targeted nutritional interventions.
Dietary factors and food contaminants may contribute risk. Improvement and loss of
diagnosis in some with ASD suggest brain circuitry amenable to environmental
modulation.
Summary: Prevalence, genetic, exposure, and pathophysiological evidence all suggest a
role for environmental factors in the inception and lifelong modulation of ASD. This
supports the need for seeking targets for early and ongoing medical prevention and
treatment of ASD.

8. *
* T Schettler (2001). Toxic threats to neurologic development of children.
Environ Health Perspect.
* Learning disabilities, attention deficit hyperactivity disorder, developmental
delays, and emotional and behavioral problems are among childhood disabilities
of increasing concern. Interacting genetic, environmental, and social factors are
important determinants of childhood brain development and function. For many
reasons, however, studying neurodevelopmental vulnerabilities in children is
challenging. Moreover, inadequate incidence and trend data interfere with full
understanding of the magnitude of the problem. Despite these difficulties,
extensive laboratory and clinical studies of several neurodevelopmental
toxicants, including lead, mercury, polychlorinated biphenyls, alcohol, and
nicotine, demonstrate the unique vulnerability of the developing brain to
environmental agents at exposure levels that have no lasting effect in adults.
Historically, understanding the effects of these toxicants on the developing brain
has emerged slowly while generations of children are exposed to unsafe levels.
Unfortunately, with few exceptions, neurodevelopmental toxicity data are
missing for most industrial chemicals in widespread use, even when
populationwide exposures are documented. The personal, family, and
communitywide costs of developmental disabilities are profound. In addition to
the need for more research, a preventive public health response requires
mitigation of exposures to potential neurodevelopmental toxicants when
available evidence establishes the plausibility of harm, despite residual
toxicologic uncertainties.

9. *
* Blaylock RL (2009).A POSSIBLE CENTRAL MECHANISM IN AUTISM SPECTRUM
DISORDERS, PART 2: IMMUNOEXCITOTOXiCITY.
* In this section, I explore the effects of mercury and inflammation on
transsulfuration reactions, which can lead to elevations in androgens, and how this
might relate to the male preponderance of autism spectrum disorders (ASD). It is
known that mercury interferes with these biochemical reactions and that
chronically elevated androgen levels also enhance the neurodevelopmental effects
of excitotoxins. Both androgens and glutamate alter neuronal and glial calcium
oscillations, which are known to regulate cell migration, maturation, and final brain
cytoarchitectural structure. Studies have also shown high levels of DHEA and low
levels of DHEA-S in ASD, which can result from both mercury toxicity and chronic
inflammation. Chronic microglial activation appears to be a hallmark of ASD.
Peripheral immune stimulation, mercury, and elevated levels of androgens can all
stimulate microglial activation. Linked to both transsulfuration problems and
chronic mercury toxicity are elevations in homocysteine levels in ASD patients.
Homocysteine and especially its metabolic products are powerful excitotoxins.
Intimately linked to elevations in DHEA, excitotoxicity and mercury toxicity are
abnormalities in mitochondrial function. A number of studies have shown that
reduced energy production by mitochondria greatly enhances excitotoxicity. Finally,
1 discuss the effects of chronic inflammation and elevated mercury levels on
glutathione and metallothionein.

10. *
How Inflammation Affects the Developing Brain
* Inflammation appears to play a role in the developing brain as the same damaging
effects of inflammatory chemical mediators of in the adult appear to cause the same
issues in the delicate brains of infants and young children.
* Recent study published in the journal BMC Pediatrics, researchers investigated
frequency of febrile illnesses in infants and blood markers of increased inflammation
* IL-1 beta, IL-6, and IL-4
* Discovered direct relationship between higher levels of inflammatory markers and risk for
developmental issues.
* Higher levels of IL-4
* is associated with lower levels of inflammation
* correlates with reduced risk for developmental issues
* authors cited “Every additional 10 days of fever is associated with:
* 1.9 decrease in language composite score
* 2.1 decrease in motor composite score.”
* Role of inflammation in brain health and function represents fundamental importance
through the age continuum.
* Re: infant health requires managing inflammation to maintain a healthy immune system/health.
* Steps to include:
* minimizing antibiotic exposure, spacing immunizations, breastfeeding, and avoiding caesarean
section
* (Retrieved from http://www.drperlmutter.com/inflammation-affects-developing-
brain/?utm_source=facebook&utm_medium=facebookpost&utm_content=bloginfantinflammation&utm_campaign=Facebook%20Posts)

11. *
* Stein J, Schettler T, Wallinga D, and Valenti M (2002). In harm's way: toxic threats to child
development.
* Developmental disabilities result from complex interactions of genetic, toxicologic (chemical), and
social factors. Among these various causes, toxicologic exposures deserve special scrutiny because
they are readily preventable. This article provides an introduction to some of the literature
addressing the effects of these toxicologic exposures on the developing brain. This body of research
demonstrates cause for serious concern that commonly encountered household and environmental
chemicals contribute to developmental disabilities. The developing brain is uniquely susceptible to
permanent impairment by exposure to environmental substances during time windows of
vulnerability. Lead, mercury, and polychlorinated biphenyls (PCBs) have been extensively studied
and found to impair development at levels of exposure currently experienced by significant portions
of the general population. High-dose exposures to each of these chemicals cause catastrophic
developmental effects. More recent research has revealed toxicity at progressively lower exposures,
illustrating a "declining threshold of harm" commonly observed with improved understanding of
developmental toxicants. For lead, mercury, and PCBs, recent studies reveal that background-
population exposures contribute to a wide variety of problems, including impairments in attention,
memory, learning, social behavior, and IQ. Unfortunately, for most chemicals there is little data
with which to evaluate potential risks to neurodevelopment. Among the 3000 chemicals produced in
highest volume (over 1 million lbs/yr), only 12 have been adequately tested for their effects on the
developing brain. This is a matter of concern because the fetus and child are exposed to untold
numbers, quantities, and combinations of substances whose safety has not been established. Child
development can be better protected by more precautionary regulation of household and
environmental chemicals. Meanwhile, health care providers and parents can play an important role
in reducing exposures to a wide variety of known and suspected neurodevelopmental toxicants that
are widely present in consumer products, food, the home, and wider community.

12. *
Mercury Exposure symptoms share
similarities w/ASD & NDD 2nd sx
* Mercury exposure at high levels harm the
brain, heart, kidneys, lungs, and immune
system across the age continuum
* Research confirms high methylmercury
blood levels in fetal & young children injure
the developing nervous system, decreasing
cognition and learning
* At high levels of exposure, methylmercury's
harmful effects on animals include
* death,
* reduced reproduction,
* slower growth & development,
* abnormal behavior.
* In utero exposure adversely affects the
fetal brain/nervous system.
* Children demonstrate deficits in:
* cognitive thinking,
* memory,
* attention,
* language,
* fine motor
* visual spatial skills
* Symptoms Methylmercury exposure:
* impairment of the peripheral vision
* disturbances in sensations
* "pins and needles" of hands, feet, peri oral
* Impaired coordination
* impaired speech, hearing, ambulation
* muscle weakness
* Symptoms high inorganic mercury exposure:
* skin rashes & dermatitis
* mood swings
* memory loss
* mental disturbances
* muscle weakness.
* Symptoms of elemental mercury effects:
* tremors
* emotional changes (mood swings, irritability,
nervousness, excessive shyness)
* insomnia
* neuromuscular changes (weakness, muscle
atrophy, twitching)
* headaches
* disturbances in sensations;
* changes in nerve responses;
* cognitive function deficits

13. *
*Methods of mercury exposure:
* Amalgam dental fillings (primary)
* Fresh water/farmed /salt water
fish (secondary)
* Some vaccines
* Industrial/work place exposures
(paint, hospital, home)
* Glass thermometers or Energy
efficient light bulbs (dropping or
breaking)
* Toxic mercury vapors released
* Computer/electronic equipment
* some cosmetics (calomel)
* Some hair bleaching products
*Classic signs of mercury poisoning
* loss of hair
* discolored fingernails
* Gums w/”Tatoo” staining from
amalgam leakage
Symptoms of human mercury poisoning
1. Psychological disturbances
* Angry fits, short term memory loss, low self
esteem, inability to sleep, loss of self-control,
sleepiness, loss of an ability to learn new
things, doing things by rote
2. Oral Cavity problems
* Inflammation of the mouth, loss of bone
around teeth, ulcerated gums and other areas
in the mouth, loose teeth, darkening of gums,
taste of metal, bleeding of gums.
3. Digestive tract problems
* Cramps, inflamed colon, GI problems, Diarrhea
and other digestive problems.
4. Cardiovascular problems
* Weak pulse, blood pressure changes, chest
pain, or feeling of pressure in the chest area.
5. Respiratory problems
* Weakness and problems with breathing,
Emphysema, Coughing persistently.
6. Neurological Problems
* Headaches, vertigo, tinnitus, shaking in various
areas of the body (eye lids, feet etc)

14. *
Mercury poisoning in Children is a cause of
many secondary sx s of ASD/NDD
Common pediatric neurological sx:
* decreased eye contact
* flat affect
* repeating certain actions over and over
again
* not responding to their name
* not looking at an object that is being
pointed at by another
* poor concentration or attention
* sensitivity to sensory stimulation
Common language/speech manifestations:
* loss of speech
* delayed speech decreased understanding
and articulating words
* remembering certain words
Common are social manifestations:
* withdrawal
* being irritated
* aggressive behavior
* night terrors
* other sleep problems
* mood swings
Other auto-immune symptoms:
* multiple sclerosis
* juvenile diabetes
* asthma
* chromic ear infections
* decreased immunity
The World Health Organization
(WHO): “there is NO KNOWN SAFE
LEVEL of mercury exposure”.
http://www.dentalwellness4u.com/layperson/symptoms.html

15. *
* Frustaci A, Neri M, Cesario A, Adams JB, Domenici E, Bernardina BD, and Bonassi S (2012).
Oxidative stress-related biomarkers in autism: Systematic review and meta-analyses.
* Autism spectrum disorders (ASDs) are rarely diagnosed in children younger than 2 years,
because diagnosis is based entirely on behavioral tests. Oxidative damage may play a central
role in this pathogenesis, together with the interconnected transmethylation cycle and
transsulfuration pathway. In an attempt to clarify and quantify the relationship between
oxidative stress-related blood biomarkers and ASDs, a systematic literature review was carried
out. For each identified study, mean biomarker levels were compared in cases and controls
providing a point estimate, the mean ratio, for each biomarker. After meta-analysis, the ASD
patients showed decreased blood levels of reduced glutathione (27%), glutathione peroxidase
(18%), methionine (13%), and cysteine (14%) and increased concentrations of oxidized
glutathione (45%) relative to controls, whereas superoxide dismutase, homocysteine, and
cystathionine showed no association with ASDs. For the C677T allele in the methylene
tetrahydrofolate reductase gene (MTHFR), homozygous mutant subjects (TT) showed a meta-OR
of 2.26 (95% CI 1.30–3.91) of being affected by ASD with respect to the homozygous nonmutant
(CC). Case-control studies on blood levels of vitamins suggest a lack of association (folic acid
and vitamin B12) or rare association (vitamins A, B6, C, D, E). Sparse results were available for
other biomarkers (ceruloplasmin, catalase, cysteinylglycine, thiobarbituric acid-reactive
substances, nitric oxide) and for polymorphisms in other genes. Existing evidence is
heterogeneous and many studies are limited by small sample size and effects. In conclusion,
existing evidence suggests a role for glutathione metabolism, the transmethylation cycle, and
the transsulfuration pathway, although these findings should be interpreted with caution, and
larger, more standardized studies are warranted.

16. *
*Allergy-an immune hyperactive response to substances considered
'foreign' to the body
* Common Allergens: food, pollen, drugs, dust
* acquired thru life
* some individuals are susceptible >others
* Requires 1 exposure to substance to become sensitized or allergic
*Conventional Medicine –
* directed to block the immune response or suppress immune function
w/steroids topically & systemically
*Naturopathic –
* identify & eliminate underlying cause verses masking symptoms
*Most allergies result from decreased mucous membranes integrity that
leak foreign substances, along w/repeat exposure to these
* weak digestion + poor diet increased volume of undigested food particles in
the gut
* Once foreign substance enters bloodstreamallergic responses triggered
* enter frequently as damaged mucous membranes unable to serve as barriers

17. *

18. *
*One carbon metabolism disturbances and the C677T MTHFR gene
polymorphism in children with autism spectrum disorders
* Autism spectrum disorders (ASDs), which include the prototypic autistic disorder (AD),
Asperger’s syndrome (AS) and pervasive developmental disorders not otherwise specified
(PDD-NOS), are complex neurodevelopmental conditions of unknown aetiology. The current
study investigated the metabolites in the methionine cycle, the transsulphuration
pathway, folate, vitamin B12 and the C677T polymorphism of the MTHFR gene in three
groups of children diagnosed with AD (n= 15), AS (n= 5) and PDD-NOS (n= 19) and their age-
and sex-matched controls (n= 25). No metabolic disturbances were seen in the AS patients,
while in the AD and PDD-NOS groups, lower plasma levels of methionine (P= 0.01 and P=
0.03, respectively) and α-aminobutyrate were observed (P= 0.01 and P= 0.001,
respectively). Only in the AD group, plasma cysteine (P= 0.02) and total blood glutathione
(P= 0.02) were found to be reduced. Although there was a trend towards lower levels of
serine, glycine, N, N-dimethylglycine in AD patients, the plasma levels of these
metabolites as well as the levels of homocysteine and cystathionine were not statistically
different in any of the ASDs groups. The serum levels of vitamin B12 and folate were in the
normal range. The results of the MTHFR gene analysis showed a normal distribution of the
C677T polymorphism in children with ASDs, but the frequency of the 677T allele was
slightly more prevalent in AD patients. Our study indicates a possible role for the
alterations in one carbon metabolism in the pathophysiology of ASDs and provides, for the
first time, preliminary evidence for metabolic and genetic differences between clinical
subtypes of ASDs (Paşca SP, Dronca E, Kaucsár T, Crǎciun EC, Endreffy E, Ferencz BK, Iftene F,
Benga I, Cornean R, Banerjee R and Dronca M; 2009).

19. *
* Currenti SA (2010). Understanding and Determining the Etiology of Autism. Cellular and
Molecular Neurobiology. March 2010, Volume 30, Issue 2, pp 161-171. Retrieved from
http://link.springer.com/article/10.1007/s10571-009-9453-8
* Worldwide, the rate of autism has been steadily rising. There are several environmental
factors in concert with genetic susceptibilities that are contributing to this rise. Impaired
methylation and mutations of mecp2 have been associated with autistic spectrum
disorders, and related Rett syndrome. Genetic polymorphisms of cytochrome P450
enzymes have also been linked to autism, specifically CYP27B1 that is essential for proper
vitamin D metabolism. Vitamin D is important for neuronal growth and
neurodevelopment, and defects in metabolism or deficiency have been implicated in
autistic individuals. Other factors that have been considered include: maternally derived
antibodies, maternal infection, heavy metal exposure, folic acid supplementation,
epigenetics, measles, mumps, rubella vaccination, and even electromagnetic radiation. In
each case, the consequences, whether direct or indirect, negatively affect the nervous
system, neurodevelopment, and environmental responsive genes. The etiology of autism
is a topic of controversial debate, while researchers strive to achieve a common
objective. The goal is to identify the cause(s) of autism to understand the complex
interplay between environment and gene regulation. There is optimism that specific
causes and risk factors will be identified. The results of future investigations will
facilitate enhanced screening, prevention, and therapy for “at risk” and autistic patients.

20. *
* Bradshaw AJL and Rinehart NJ (2005). Autism and Asperger's disorder: Are they
movement disorders involving the cerebellum and/or basal ganglia? Brain Research
Bulletin Volume 67, Issue 4, 30 October 2005, Pages 327–334
*Autism and Asperger's disorder (AD) are childhood developmental disorders of
unknown etiology. Autism and AD share several behavioral features, and it is not clear
whether they are distinct disorders or variants of the same disorder. Recent studies
indicate that disordered movement may be another feature of autism and AD, and
that this may reflect dysfunction within the frontostriatal and/or cerebellar motor
circuits. While disordered movement in autism and AD has been examined in a variety
of ways, it is relatively under-researched compared to the cognitive, affective, and
behavioral disturbances seen in these disorders. This review examines the role of the
frontostriatal and cerebellar motor systems in the behavioral features of autism and
AD, with gait as a proxy, and discusses difficulties with their diagnosis and their
possible pathogenesis.

21. *

22. *

23. *
*Sleep disorders are more common in persons with ASD
*Sleep Disorders include:
* Difficulty falling asleep
* Inconsistent sleep routines
* Restlessness or poor sleep quality
* Waking early, frequently, and abruptly
* increased sensitivity to outside stimuli (touch or sound)
*Studies demonstrate children with ASD fail to release melatonin at the
correct day times hours causing high levels of melatonin during the day
and lower levels when they need it at night
* Commonly, melatonin levels rise in response to darkness and dip during the
daylight hours
*Melatonin requires an amino acid tryptophan, which research has also
discovered is either higher or lower than normal in ASD children
*Anxiety is secondary symptom that may adversely affect sleep.
* ASD Children tend to test higher than other children for anxiety

24. *
* “Individuals with autism also have gifts. The gifts of autism occur as a
result of the strong visual abilities, attention to minute details,
unusual interests, and amazing memory. Other common traits, such as
honesty, naivetè, gentleness, compliance, and perfectionism, are
exceedingly refreshing and unexpected in this increasingly cynical
world”
Janzen, J. E. (1999). Autism: Facts and strategies for Parents, p. 151.

25. *
*No big smiles or other warm, joyful expressions
by six months or thereafter
*No back-and-forth sharing of sounds, smiles or
other facial expressions by nine months
*No babbling by 12 months
*No back-and-forth gestures such as pointing,
showing, reaching or waving by 12 months
*No words by 16 months
*No meaningful, two-word phrases (not
including imitating or repeating) by 24 months
*Any loss of speech, babbling or social skills at
any age

26. *
*“The major source of stress in life for the person
with Asperger's Syndrome is social contact, and
increased stress generally leads to anxiety
disorders and depression”
Attwood, T. Asperger's Syndrome: A Guide for Parents
and Professionals, 1998, p. 148.

27. *
* McAlonan GM, Daly E, Kumari V, Critchley HD, van Amelsvoort T, Suckling J, Simmons A,
Sigmundsson T, Greenwood K, Russell A, Schmitz N, Happe F, Howlin P and Murphy DGM
(2002). Brain anatomy and sensorimotor gating in Asperger’s syndrome.
* Asperger’s syndrome (an autistic disorder) is characterized by stereotyped and obsessional
behaviors, and pervasive abnormalities in socio‐emotional and communicative behavior.
These symptoms lead to social exclusion and a significant healthcare burden; however, their
neurobiological basis is poorly understood. There are few studies on brain anatomy of
Asperger’s syndrome, and no focal anatomical abnormality has been reliably reported from
brain imaging studies of autism, although there is increasing evidence for differences in
limbic circuits. These brain regions are important in sensorimotor gating, and impaired
‘gating’ may partly explain the failure of people with autistic disorders to inhibit repetitive
thoughts and actions. Thus, we compared brain anatomy and sensorimotor gating in healthy
people with Asperger’s syndrome and controls. We included 21 adults with Asperger’s
syndrome and 24 controls. All had normal IQ and were aged 18–49 years. We studied brain
anatomy using quantitative MRI, and sensorimotor gating using prepulse inhibition of startle
in a subset of 12 individuals with Asperger’s syndrome and 14 controls. We found significant
age‐related differences in volume of cerebral hemispheres and caudate nuclei (controls, but
not people with Asperger’s syndrome, had age‐related reductions in volume). Also, people
with Asperger’s syndrome had significantly less grey matter in frontostriatal and cerebellar
regions than controls, and widespread differences in white matter. Moreover, sensorimotor
gating was significantly impaired in Asperger’s syndrome. People with Asperger’s syndrome
most likely have generalized alterations in brain development, but this is associated with
significant differences from controls in the anatomy and function of specific brain regions
implicated in behaviors characterizing the disorder. We hypothesize that Asperger’s syndrome
is associated with abnormalities in frontostriatal pathways resulting in defective
sensorimotor gating, and consequently characteristic difficulties inhibiting repetitive
thoughts, speech and actions.

28. *
*Asperger Syndrome is a developmental disorder characterized
by:
*repetitive routines or rituals,
*peculiarities in speech/language (overly formal speech or monotone,
or takes speech literally)
*socially & emotionally inappropriate behavior
*inability to interact successfully with peers
*problems with non-verbal communication,
*restricted use of gestures
*limited or inappropriate facial expressions
*peculiar, stiff gaze
*Clumsiness and uncoordinated motor movements

29. *
*(characteristics cont.)
*intelligence appeared normal,
*lacked nonverbal communication skills,
*failed to demonstrate empathy with their peers,
*speaking disjointed or overly formal,
*Demonstrates all absorbing interest in a single topic which
dominates their conversations
*Individuals who are diagnosed with autism or autism spectrum
disorder who have normal cognitive abilities, and experienced
no significant delay in acquiring language skills, are very similar
to individuals with High Functioning Autism Spectrum Disorder
(HFA) and Asperger Syndrome share similar symptoms and are
helped by similar treatment approaches.

30. *
* AS may be hard to differentiate from those of other behavioral issues like attention deficit
hyperactivity disorder (ADHD)
* An ADHD diagnosis may be later changed to AS when issues appear to be caused more by the
inability to socialize instead of an inability to focus.
* Common AS sx:
* improper of very few social interactions
* "robotic" or repetitive speech
* average or below average nonverbal communication skills, yet average or above average verbal
communications skills
* tendency to discuss self rather than others
* inability to understand issues or phrases that are considered "common sense"
* lack of eye contact or reciprocal conversation
* obsession with specific unique topics
* one-sided conversations
* awkward movements and/or mannerisms
* inability to understand the actions, words or behaviors of other people
* often don’t understand humor or the implications of particular phrases or actions of other people
* unable to see the relationship between these nonverbal communication methods, and verbal
methods like speech and language
* have difficulty seeing things from another person’s perspective
* Difficulty regluating their emotions

31. *
*"Sensory Integration is the ability to take in information through
senses,...to put it together with prior information, memories and
knowledge stored in the brain, and to make a meaningful response.“
The SPD child may frequently respond to or register sensory
information without the ability to screen out nonessential sensory
information, or the child may fail to register the input from one or
more senses.

32. *
Miller LJ and Schaaf RC (2008). Sensory Processing Disorder
* Sensory processing disorder (SPD) is a complex developmental disorder affecting
children and adults. These people over-respond, under-respond, excessively
crave/seek out intense sensory experiences, have difficulty discriminating
sensation, or respond to sensory input in an atypical manner, impacting their
daily life activities. Sensory integration theory was developed by Dr. A. Jean
Ayres in the 1970s and 1980s. This article updates the theory and presents a new
taxonomy to classify SPD into three classic patterns: sensory modulation
disorder, sensory discrimination disorder, and sensory-based motor disorder.
Intervention for SPD, occupational therapy using a sensory integrative approach,
is briefly described. A brief review of intervention effectiveness studies is
presented in this article.
Reisman J (2008). Sensory processing disorders. Minnesota Medicine [2002,
85(11):48-51] Retrieved from http://europepmc.org/abstract/MED/12498067
* Most people are able to effectively process and respond to the sensory stimuli of
daily life. But people who have sensory processing disorders struggle to form
meaningful responses to sensory stimuli. As a result these individuals often
exhibit problems with coordination, sensory-seeking or sensory-avoiding
behaviors, and sensory modulation.

33. *
Effects of Disordered Sensory
Integration (SPD)
* Distractible, hyperactive, uninhibited
* Behavior Problems
* Poor Speech Development
* Difficulty establishing sleeping and
eating patterns
* Disorders of muscle tone
* Poor Gross and/or Fine Motor
Coordination
* Learning disabilities
* Social problems
* Unable to calm or console themselves
* Irritable, difficult to soothe,
emotionally liable
* Hypersensitive to touch
* Aggressive
* Avoidant, withdrawing
* Intolerant of daily routines
* Rigid about textures, "feel"
* Hypersensitive to auditory, visual,
olfactory,vestibular stimuli
* Lacks purpose in activity
* Often does not manipulate toys or
play with them creatively
* Often does not explore the
environment
* Plays very repetitively with toys
* Prefers only one type of activity
* Seeks excessive or vigorous sensory
input
* "Fight, flight, or fright” response to
sensory information most people
would consider harmless

34. *
*A high incidence of sensory processing difficulties exists in children with Autism
Spectrum Disorder (ASD) and children with Sensory Modulation Disorder (SMD)
* (Schoen SA, Miller LJ Brett-Green BA and Nielsen DM, 2009).
*Unusual sensory processing has been widely reported in autism spectrum
disorders (ASDs); however, the majority of research in this area has focused on
children. The present study assessed sensory processing in adults with ASD
using the Adult/Adolescent Sensory Profile (AASP), a 60-item self-report
questionnaire assessing levels of sensory processing in everyday life. Results
demonstrated that sensory abnormalities were prevalent in ASD, with 94.4
percent of the ASD sample reporting extreme levels of sensory processing on at
least one sensory quadrant of the AASP. Furthermore, analysis of the patterns
of sensory processing impairments revealed striking within-group variability in
the ASD group, suggesting that individuals with ASD could experience very
different, yet similarly severe, sensory processing abnormalities. These results
suggest that unusual sensory processing in ASD extends across the lifespan and
have implications regarding both the treatment and the diagnosis of ASD in
adulthood.
* Crane L, Goddard L, and Pring L. (2009). Sensory processing in adults with autism
spectrum disorders.

35. *

36. *
Inflammation: good or bad for ADHD? ADHD Attention Deficit and Hyperactivity Disorders
* Attention deficit hyperactivity disorder (ADHD) is characterized by the typical behavioral core
symptoms of inattentiveness, hyperactivity and impulsiveness. ADHD is a usually chronic health
conditions, mostly diagnosed in childhood, creating a significant challenge for youth, their families and
professionals who treat it. This disorder requires long-term treatments, including psychotherapeutic
and pharmacological interventions, which in some cases may lead to adverse effects. Understanding
the mechanism by which ADHD risk factors affect the biochemical processes in the human brain and
consequentially the behavior will help to identify novel targets for the development of therapeutics
with less adverse results and better efficacy including higher responder rates. Although inflammatory
responses in the brain have been recognized for years as critical in neurodegeneration and behavior in
a number of neurological and psychiatric disorders, their role for the development, treatment and
prevention of ADHD has been so far largely overlooked, although historically, ADHD symptoms were
initially observed in patients who survived an ONJ infection, i.e. inflammation. In this review, we
discuss the interrelationship between different ADHD risk factors and inflammation with respect to the
triggered molecular mechanisms and the contribution they are likely to have to this disorder. This
paper provides a rationale for future studies on ADHD with an intent to inspiring the development of
new agents for a more efficient management of this disorder (Doney and Thome, 2010).
* “According to the Centers for Disease Control, greater than 9 percent of children in the United States
suffer from ADHD (1). This is approximately half the percentage of children who are obese (2). I
suggest that both conditions are related to increased inflammation induced by radical changes in the
American diet during the past 40 years” (Sears, 2011).

37. *
* Mangeot SD, Miller LJ, McIntosh DN, McGrath-Clarke J, Simon J, Hagerman RJ and
Goldson E (2001). Sensory modulation dysfunction in children with attention-deficit-
hyperactivity disorder.
* This study investigates the presence of sensory modulation dysfunction (SMD) among
children with attention-deficit-hyperactivity disorder (ADHD). Twenty-six children with
ADHD (mean age 8.3 years, 18 males, 8 females), and 30 typically developing children
(mean age 8.2 years, 21 males, 9 females) were tested using a laboratory procedure
that gauges responses to repeated sensory stimulation by measuring electrodermal
reactivity (EDR). Parental report measures of limitations in sensory, emotional, and
attentional dimensions were administered using the Short Sensory Profile, the Leiter
International Performance Scale-Revised, Parent Rating subscales, and the Child
Behavior Checklist (CBCL). Compared to the typical sample, the children with ADHD
displayed greater abnormalities in sensory modulation on both physiological and parent-
report measures. The children with ADHD also displayed more variability in responses.
Within the group with ADHD, levels of SMD were highly correlated with measures of
psychopathology on the CBCL. Implications of findings relate to the importance of
considering sensory processing abilities in a subgroup of children with ADHD.

38. *
*While Homeobotanicals (Hb)
formulas do not cure sx of
ASD or NDD, they can lessen
or soften 2nd symptoms:
*Hb A (Allergy)
*Hb B (Blood Purifier)
*Hb E (Emotion/Stress)
*Hb D & G (Digestion & GI)
*Hb Z (Sleep)
*Hb Q (quiet/calm)
*Hb I (Immune/Infection)
*Hb T (Tired)
*Hb Detoxa
*Hb First Aid
*Hb Marina
*Hb Nutria
*Hb Promyer
*Hb Serena

39. *
* 1.Organic Diet-
* minimizes damage to intestinal lining
* provides required nutrients for intestinal regeneration
* Strengthens intestinal & respiratory mucous membrane integrity
* 2. Avoid eating same foods daily
* practice variety & rotation—decreases repeated contact with same foreign substances
* decreasing acquiring allergies.
* 3. Use dietary antioxidant supplements –
* assist mucous membranes' integrity
* prevent damage
* 4.Minimize environmental chemicals & toxin exposure (they overload the immune system)
* including:
* Heavy metal exposure (mercury, lead, aluminum)
* food additives/preservatives/colors/sugars
* cleaning materials/detergents
* Pesticides
* immunizations
* Paints
* 5. cleansing/detox program
* 6. Avoid immunizations or limit exposure by spacing out 1 per time

40. *
* Autism Speaks (2014). What is Autism/Autism Spectrum Disorders? http://www.autismspeaks.org/what-autism.
* http://www.hbci.com/~wenonah/new/9steps.htm
* Bradshaw AJL and Rinehart NJ (2005). Autism and Asperger's disorder: Are they movement disorders involving the
cerebellum and/or basal ganglia? Brain Research Bulletin Volume 67, Issue 4, 30 October 2005, Pages 327–334
* Blaylock RL (2009).A POSSIBLE CENTRAL MECHANISM IN AUTISM SPECTRUM DISORDERS, PART 2: IMMUNOEXCITOTOXiCITY.
Alternative Therapies in Health & Medicine . Jan/Feb2009, Vol. 15 Issue 1, p60-67. 8p Retrieved from
http://web.a.ebscohost.com/abstract?direct=true&profile=ehost&scope=site&authtype=crawler&jrnl=10786791&AN=375
70226&h=JpN2y%2b%2b6SmKzaEfH1cPa1eANggO0w08mWWjMYLQxcg%2bWBhvSuZfQYjDUcrc6X4kJcWZUXifdmHGXgGQrkC
c9tQ%3d%3d&crl=c
* Doney R and Thome J (2010). Inflammation: good or bad for ADHD? ADHD Attention Deficit and Hyperactivity Disorders
December 2010, Volume 2, Issue 4, pp 257-266 Retrieved from http://link.springer.com/article/10.1007/s12402-010-
0038-7.
* Dunn, Winnie; Bennett, Donna (). Patterns of sensory processing in children with attention deficit hyperactivity disorder.
Occupational Therapy Journal of Research, Vol 22(1), 2002, 4-15.Retrieved from http://psycnet.apa.org/psycinfo/2002-
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* Crane L, Goddard L, and Pring L. (2009). Sensory processing in adults with autism spectrum disorders. doi:
10.1177/1362361309103794 Autism May 2009 vol. 13 no. 3 215-228. Retrieved from
http://aut.sagepub.com/content/13/3/215.short
* Currenti SA (2010). Understanding and Determining the Etiology of Autism. Cellular and Molecular Neurobiology. March
2010, Volume 30, Issue 2, pp 161-171. Retrieved from http://link.springer.com/article/10.1007/s10571-009-9453-8
* Frustaci A, Neri M, Cesario A, Adams JB, Domenici E, Bernardina BD, and Bonassi S (). Oxidative stress-related
biomarkers in autism: Systematic review and meta-analyses. Free Radical Biology and Medicine. Volume 52, Issue 10, 15
May 2012, Pages 2128–2141 Retrieved from
http://www.sciencedirect.com/science/article/pii/S0891584912001827http://www.sciencedirect.com/science/article/
pii/S0891584912001827
* Herbert MR (2010). Contributions of the environment and environmentally vulnerable physiology to autism spectrum
disorders. Current Opinion in Neurology: April 2010 - Volume 23 - Issue 2 - p 103–110. doi:
10.1097/WCO.0b013e328336a01f. Developmental disorders: Edited by Geraldine Dawson. Retrieved from
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41. *
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*