The Cure for Attention Deficit Disorder was Right Under Your Nose! - PowerPoint PPT Presentation


Title: The Cure for Attention Deficit Disorder was Right Under Your Nose!


1
The Cure for Attention Deficit Disorder was Right
Under Your Nose!
-An argument supporting a dietary solution for
Attention Deficit Disorder
By Elizabeth Huser
2
Attention Deficit Disorder Defined
  • a persistent pattern of inattention and/or
    hyperactivity-impulsivity that is more frequent
    and severe than is typically observed in
    individuals at a comparable level of development
  • - American Psychiatric Association Staff

3
Diagnosing Attention Deficit Disorder
  • In order to be deemed pathological by the
    diagnosing physician
  • Symptoms must appear before age 7
  • Symptoms must persist for at least 6 months
  • Symptoms must appear in two settings
  • Work
  • School
  • Home

4
ADD is not simply an inability to sit still
  • 1/2 of those with ADD during adolescence have ADD
    into adulthood
  • Emotional, Social, and Family Problems
  • Depressed Academic and Professional Performance
  • 50 of children diagnosed ADD exhibit other
    psychiatric disorders later in life
  • Higher risk for delinquency and substance abuse

5
Many are affected
  • 1993 2 million people diagnosed ADD
  • 2000 ADD was responsible for 30-50 of mental
    health service referrals for children
  • 2000 4 million people diagnosed ADD
  • 2004 2-6 of school-age children diagnosed ADD

6
International Classification of Disease Revised
Edition
  • ADD is a neurological impairment which is
    categorized as a metabolic encephalopathy that
    affects the release and homeostasis of
    neurotransmitters.

7
The Brain in ADD
Brain activity Without ADHD
Brain activity With ADHD
The ADHD brain exhibits less activity in areas
that control Attention according to Dr. Alan
Zametkin
8
PET data applied to ADD Pathology
  • In 1993 Zametkin et al. found a negative
    correlation between frontal lobe brain activity
    and symptom severity in 10 ADHD adolescents

9
Frontostriatal circuitry and possibly
intracortical connections via the corpus callosum
are responsible for the neuropsychological
deficits associated with ADD
10
The neuro-anatomical quirks from brain imaging
studies are in regions essential to dopamine
production
  • The abnormal neuroanatomy has not been proven to
    be pathological
  • Currently, hypo-efficient dopamine systems seem
    to be the essence of ADD pathology

11
Treatment with Pharmaceuticals
  • First line of stimulants commonly prescribed
    include methylphenidates such as
  • - Ritalin
  • - Amphetamines
  • - Adderall
  • -Dexedrine

In the year 2000 there were already between 1.5
and 3 million ADHD children taking
methylphenidates
12
Stimulants Restore Normal Brain Activity
http//www.brain-dynamics.net/research/clin_files
/clin_images/adhd_spam.jpg
13
Low dopamine causes inattention and hyperactivity
which collectively are referred to as Attention
Deficit Disorder
14
Etiology of ADD
Neurodevelopmental damage from Environmental and
Heavy metal Toxicity as well has genetic flaws
Are thought to cause ADD
15
Genetic Predisposition
  • Familial incidence of ADD is common
  • Characteristic polymorphisms of dopamine-related
    genes in individuals with ADD
  • COMT is an enzyme that degrades dopamine
  • Valine is an allele for the COMT gene that
    confers higher catabolic activity of the enzyme -
    less dopamine availability.
  • Egan et al. reported a correlation between the
    valine/valine genotype and depressed dorsolateral
    prefrontal cortex activity
  • Low dopamine may also be due to
  • Impaired vesicular storage of dopamine
  • Inadequate dopamine synthesis
  • Inadequate dopamine release
  • Therefore, current research supports a polygenic
    mode of inheritance

16
Studies support other risk factor categories
  • Food and additive allergies
  • Low protein/high carbohydrate
  • Mineral imbalances
  • Essential fatty acid and phospholipid
    deficiencies
  • Thyroid disorders
  • B-vitamin deficiencies
  • Phytonutrient deficiencies
  • Amino Acid deficiencies

17
Combining it all
18
People with ADD may be genetically predisposed to
amino acid deficiency
  • Bornstein et al. reported that 28 ADD subjects
    had significantly lower levels of phenylalanine,
    tyrosine, tryptophan, histidine, and isoleucine
    than the 20 control subjects

19
Amino Acid deficiency is clearly consistent with
the pathology of ADD
  • Dopamine and norepinephrine are synthesized from
    either phenylalanine or tyrosine
  • Tryptophan is a substrate for serotonin

20
Without sufficient precursor levels,
neurotransmitter production is severely limited
21
Amino Acid Supplementation Augments
Neurotransmitter levels and alleviates ADD
symptoms
  • Theanine administration was accompanied by
    significant increases in serotonin and dopamine
    concentrations without apparent initial
    deficiency
  • (Yokogoshi et al. 1998)
  • L-tyrosine supplementation resulted in increased
    levels of both central dopamine and
    norepinephrine in rats
  • (McConnell 1985)
  • 2-week, double-blind crossover study of
    DL-Phenylalanine vs. Placebo in 19 ADD patients
  • Mean global rating of improvement in experimental
    subjects approached significance as compared with
    the control group
  • (Wood et al. 1985)

22
Long Term Effects of Amphetamines?
  • The mechanistic action and chemical structure of
    stimulants used for ADD treatment and illegal
    recreational stimulants are extremely similar.
  • Thus, stimulants used for ADD symptom management
    are extremely addictive. They are a Schedule II
    controlled substance in the United States.
  • Physicians Desk Reference Sufficient data on
    saftey and efficacy of long-term use of
    methylphenidate in children are not yet
    available
  • With the limited knowledge of the potential
    dangers of stimulant therapy, it is logical to
    rule out these other biological risk factors
    prior to subjecting a child to pharmaceutical
    treatment
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The Cure for Attention Deficit Disorder was Right Under Your Nose!

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The Cure for Attention Deficit Disorder was Right Under Your Nose!-An argument supporting a dietary solution for Attention Deficit Disorder By: Elizabeth Huser – PowerPoint PPT presentation

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Title: The Cure for Attention Deficit Disorder was Right Under Your Nose!


1
The Cure for Attention Deficit Disorder was Right
Under Your Nose!
-An argument supporting a dietary solution for
Attention Deficit Disorder
By Elizabeth Huser
2
Attention Deficit Disorder Defined
  • a persistent pattern of inattention and/or
    hyperactivity-impulsivity that is more frequent
    and severe than is typically observed in
    individuals at a comparable level of development
  • - American Psychiatric Association Staff

3
Diagnosing Attention Deficit Disorder
  • In order to be deemed pathological by the
    diagnosing physician
  • Symptoms must appear before age 7
  • Symptoms must persist for at least 6 months
  • Symptoms must appear in two settings
  • Work
  • School
  • Home

4
ADD is not simply an inability to sit still
  • 1/2 of those with ADD during adolescence have ADD
    into adulthood
  • Emotional, Social, and Family Problems
  • Depressed Academic and Professional Performance
  • 50 of children diagnosed ADD exhibit other
    psychiatric disorders later in life
  • Higher risk for delinquency and substance abuse

5
Many are affected
  • 1993 2 million people diagnosed ADD
  • 2000 ADD was responsible for 30-50 of mental
    health service referrals for children
  • 2000 4 million people diagnosed ADD
  • 2004 2-6 of school-age children diagnosed ADD

6
International Classification of Disease Revised
Edition
  • ADD is a neurological impairment which is
    categorized as a metabolic encephalopathy that
    affects the release and homeostasis of
    neurotransmitters.

7
The Brain in ADD
Brain activity Without ADHD
Brain activity With ADHD
The ADHD brain exhibits less activity in areas
that control Attention according to Dr. Alan
Zametkin
8
PET data applied to ADD Pathology
  • In 1993 Zametkin et al. found a negative
    correlation between frontal lobe brain activity
    and symptom severity in 10 ADHD adolescents

9
Frontostriatal circuitry and possibly
intracortical connections via the corpus callosum
are responsible for the neuropsychological
deficits associated with ADD
10
The neuro-anatomical quirks from brain imaging
studies are in regions essential to dopamine
production
  • The abnormal neuroanatomy has not been proven to
    be pathological
  • Currently, hypo-efficient dopamine systems seem
    to be the essence of ADD pathology

11
Treatment with Pharmaceuticals
  • First line of stimulants commonly prescribed
    include methylphenidates such as
  • - Ritalin
  • - Amphetamines
  • - Adderall
  • -Dexedrine

In the year 2000 there were already between 1.5
and 3 million ADHD children taking
methylphenidates
12
Stimulants Restore Normal Brain Activity
http//www.brain-dynamics.net/research/clin_files
/clin_images/adhd_spam.jpg
13
Low dopamine causes inattention and hyperactivity
which collectively are referred to as Attention
Deficit Disorder
14
Etiology of ADD
Neurodevelopmental damage from Environmental and
Heavy metal Toxicity as well has genetic flaws
Are thought to cause ADD
15
Genetic Predisposition
  • Familial incidence of ADD is common
  • Characteristic polymorphisms of dopamine-related
    genes in individuals with ADD
  • COMT is an enzyme that degrades dopamine
  • Valine is an allele for the COMT gene that
    confers higher catabolic activity of the enzyme -
    less dopamine availability.
  • Egan et al. reported a correlation between the
    valine/valine genotype and depressed dorsolateral
    prefrontal cortex activity
  • Low dopamine may also be due to
  • Impaired vesicular storage of dopamine
  • Inadequate dopamine synthesis
  • Inadequate dopamine release
  • Therefore, current research supports a polygenic
    mode of inheritance

16
Studies support other risk factor categories
  • Food and additive allergies
  • Low protein/high carbohydrate
  • Mineral imbalances
  • Essential fatty acid and phospholipid
    deficiencies
  • Thyroid disorders
  • B-vitamin deficiencies
  • Phytonutrient deficiencies
  • Amino Acid deficiencies

17
Combining it all
18
People with ADD may be genetically predisposed to
amino acid deficiency
  • Bornstein et al. reported that 28 ADD subjects
    had significantly lower levels of phenylalanine,
    tyrosine, tryptophan, histidine, and isoleucine
    than the 20 control subjects

19
Amino Acid deficiency is clearly consistent with
the pathology of ADD
  • Dopamine and norepinephrine are synthesized from
    either phenylalanine or tyrosine
  • Tryptophan is a substrate for serotonin

20
Without sufficient precursor levels,
neurotransmitter production is severely limited
21
Amino Acid Supplementation Augments
Neurotransmitter levels and alleviates ADD
symptoms
  • Theanine administration was accompanied by
    significant increases in serotonin and dopamine
    concentrations without apparent initial
    deficiency
  • (Yokogoshi et al. 1998)
  • L-tyrosine supplementation resulted in increased
    levels of both central dopamine and
    norepinephrine in rats
  • (McConnell 1985)
  • 2-week, double-blind crossover study of
    DL-Phenylalanine vs. Placebo in 19 ADD patients
  • Mean global rating of improvement in experimental
    subjects approached significance as compared with
    the control group
  • (Wood et al. 1985)

22
Long Term Effects of Amphetamines?
  • The mechanistic action and chemical structure of
    stimulants used for ADD treatment and illegal
    recreational stimulants are extremely similar.
  • Thus, stimulants used for ADD symptom management
    are extremely addictive. They are a Schedule II
    controlled substance in the United States.
  • Physicians Desk Reference Sufficient data on
    saftey and efficacy of long-term use of
    methylphenidate in children are not yet
    available
  • With the limited knowledge of the potential
    dangers of stimulant therapy, it is logical to
    rule out these other biological risk factors
    prior to subjecting a child to pharmaceutical
    treatment
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