Embed Size (px)
Citation preview
The Cure for Attention Deficit Disorder was Right Under
Your Nose!
The Cure for Attention Deficit Disorder was Right Under
Your Nose!
By: Elizabeth Huser
-An argument supporting a dietary solution for Attention Deficit Disorder
Attention Deficit Disorder Defined:Attention Deficit Disorder Defined:Attention Deficit Disorder Defined: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
“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
Diagnosing Attention Deficit Disorder: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
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
ADD is not simply an inability to ADD is not simply an inability to sit still…sit still…
ADD is not simply an inability to ADD is not simply an inability to sit still…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
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
Many are affected…Many are affected…Many are affected…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
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
International Classification of Disease Revised Edition:
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.
ADD is a neurological impairment which is categorized as a
“metabolic encephalopathy” that affects the release and
homeostasis of neurotransmitters.
The Brain in ADDThe Brain in ADD
Brain activity Without ADHD
Brain activityWith ADHD
The ADHD brain exhibits less activity in areas that control Attention according to Dr. Alan Zametkin
PET data applied to ADD Pathology
PET data applied to ADD Pathology
Symptom Severity vs. Brain ActivitySymptom Severity vs. Brain Activity
In 1993 Zametkin et al. found a negative correlation between frontal lobe brain activity and symptom severity in 10 ADHD adolescents
In 1993 Zametkin et al. found a negative correlation between frontal lobe brain activity and symptom severity in 10 ADHD adolescents
Frontostriatal circuitry and possibly intracortical connections via the corpus callosum are responsible for the neuropsychological
deficits associated with ADD
Frontostriatal circuitry and possibly intracortical connections via the corpus callosum are responsible for the neuropsychological
deficits associated with ADD
The neuro-anatomical quirks from brain imaging studies are in regions essential
to dopamine production
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
The abnormal neuroanatomy has not been proven to be pathological
Currently, hypo-efficient dopamine systems seem to be the essence of ADD pathology
Treatment with PharmaceuticalsTreatment with Pharmaceuticals
First line of stimulants commonly prescribed include methylphenidates such as:
- Ritalin
- Amphetamines
- Adderall
-Dexedrine
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
Stimulants Restore Normal Brain ActivityStimulants Restore
Normal Brain Activity
http://www.brain-dynamics.net/research/clin_files/clin_images/adhd_spam.jpg
Low dopamine causes inattention and hyperactivity which
collectively are referred to as Attention Deficit Disorder
Low dopamine causes inattention and hyperactivity which
collectively are referred to as Attention Deficit Disorder
Inattention Hyperactivity
Attention Deficit Disorder
Low Dopamine
Hypo-efficient Dopamine Systems
Inattention Hyperactivity
Attention Deficit Disorder
Low Dopamine
Hypo-efficient Dopamine Systems
Etiology of ADDEtiology of ADD
Neurodevelopmental damage fromEnvironmental and Heavy metal Toxicity as well has genetic flaws Are thought to cause ADD
Genetic PredispositionGenetic 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
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
Studies support other risk factor categories
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
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
Combining it all… Combining it all…
Heavy Metal Toxicity(Neurodevelopmental Damage)
Inattention Hyperactivity
Attention Deficit Disorder
Low Dopamine
Hypo-efficient Dopamine Systems
Environmental Toxins(Neurodevelopmental Damage)
Congenital Causes(genes that directly code forfaulty dopamine systems)
(predisposition to nutrient imbalances etc.)
Heavy Metal Toxicity(Neurodevelopmental Damage)
Inattention Hyperactivity
Attention Deficit Disorder
Low Dopamine
Hypo-efficient Dopamine Systems
Environmental Toxins(Neurodevelopmental Damage)
Congenital Causes(genes that directly code forfaulty dopamine systems)
(predisposition to nutrient imbalances etc.)
People with ADD may be genetically predisposed to amino acid deficiencyPeople 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
Bornstein et al. reported that 28 ADD subjects had significantly lower levels of
phenylalanine, tyrosine, tryptophan, histidine, and isoleucine than the 20 control subjects
Amino Acid deficiency is clearly consistent with the pathology of ADD
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
Dopamine and norepinephrine are synthesized from either phenylalanine or tyrosine
Tryptophan is a substrate for serotonin
Without sufficient precursor levels, neurotransmitter
production is severely limited
Without sufficient precursor levels, neurotransmitter
production is severely limited
Amino Acid Supplementation Augments Neurotransmitter levels and alleviates ADD
symptoms
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)
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)
Long Term Effects of Amphetamines?
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.
Physician’s 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
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.
Physician’s 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
