Hyperactivity or hyperkineses, as the
name implies (hyper from the Greek, meaning over and above;
from the Latin to act; and kinesis from the Greek, meaning
motion), is a condition of abnormal or excessive activity,
such as that manifested in the manic, or up, phase of manic-depressive
states. As a descriptive term, it may be a symptom of some
disease states such as hyperthyroidism (over-active thyroid
gland); some medications and drugs, such as those commonly
known as "uppers" (amphetamines); and other chemicals
such as caffeine.
Earlier the term "hyperactivity" referred to a specific
syndrome characterized by excessive motor (muscular and motion)
activity, and the inability to sit still and/or keep the attention
focused on one subject for very long. Recently, we have been
using terms, such as "Attention Deficit-Hyperactivity
Whatever the case may be, the terms hyperactivity and ADHD,
whether used alone or with the word "syndrome" usually
refer to a condition ascribed to children. However, it is our
contention that the conditions apply to individuals of all
What distinguishes the hyperactive individual from the normally
active. Unfortunately, there is no simple definition. In contrast
to normally active children, hyperactive individuals exhibit
purposeless activity. They usually cannot sit still. They cannot
sit through a meal, watch an entire television program, listen
to the end of a story, pay attention in school, complete a
chore or assignment. They are always fidgeting, wiggling in
their chairs, or moving about. They appear to be in perpetual
Unlike an extremely active normal child, the activity of the
hyperactive individual usually does not result in any meaningful
accomplishments. Since they cannot sit still in school, they
do not pay attention. Their attention span is poor. They fail
in school or bring home poor grades. It is usually at this
time that parents become really concerned ñ when their
childís hyperactivity is translated to poor performance
and grades in school.
The diagnosis can be either made most easily or be difficult
to ascertain. Hyperkinetic children my exhibit the above-described
performance. Additionally, they may be clumsy; they may cry,
complain, seem depressed and unhappy, appear sullen at times
or angry. They usually are disciplinary problems because thay
may act hostile and be into almost anything and everything.
They never stop. They tend to drive their parents, teachers,
and babysitters "up the wall." Mothers complain of
constantly being exhausted and that they seem to get anything
done because their hyperkinetic children require constant attention.
Fathers, on the other hand, rarely see the problem, although
the more perceptive may. Fathers usually get involved later
when the childís hyperactive behavior is translated
into poor grades.
The, all of a sudden, things become different. The teachers
are blamed and controversy arises from the lack of understanding
of what is really happening.
A complex condition, such as hyperactivity, usually has many
causative or aggravating factors, many of which may not be
operative at the same time. Among the many related causes one
- Diet (sugar, food additives, flavors and dyes, caffeine-containing
drinks and foods, milk, etc.)
- Food allergy and sensitivity.
- Environmental chemical sensitivities.
- Increased phosphate intake from usually from foods.
- Magnesium deficiency.
- Vitamin deficiencies, especially the B vitamins.
- Heavy metal toxicity (lead, cadmium): symptoms of impaired
behavior and learning from even low level lead poisoning
include: distract ability, daydreaming, impulsiveness, lack
of persistence, constantly dependent and clinging, easily
frustrated, failure to follow simple directions, failure
to follow sequence of direction, less competent in areas
of verbal performance and auditory processing, impaired ability
to sustain attention, performance significantly poorer on
the Weschler Intelligence Scale for children.
- Lack of full spectrum light.
- Lack of appropriate discipline.
THOUGHTS ABOUT ATTENTION
DEFICIT DISORDER (ADD), AUTISM, AND BIPOLAR DISEASE
by nicola michael c. Tauraso, M.D., F.A.A.P.
What prompts me to write this dissertation
is that several nights ago I attended a lecture given by a
National Institutes of Health physician who spouted his research
on Bipolar Disease in children. I asked the question whether
he was aware of individuals performing studies on the role
of nutrition as one of the potential influencing causes and
as possible method of treatment of bipolar disease. After listening
to his lecture for over one and a quarter hours, I was not
surprised when he answered that, although he was aware that
perhaps others were involved in these pursuits, his research
involved another approach.
During his talk he described some differences between bipolar
disease and other manifestations of childhood aberrant behavior,
such as hyperactivity and attention deficit disorder (ADD)
which is now being referred to as Attention Deficit-Hyperactivity
Disorder (ADHD). It seems that with the passage of time physicians
keep changing the names of these diseases to accommodate
both changes in reclassification and to be more politically
Evidence for the latter is when the term "minimal brain
dysfunction" (MBD) was being used. When individuals decided
that no one wanted to be labeled as "minimally brain dysfunctioned," we
quickly changed the name to a less emotionally charge term.
Also during his talk, this NIH researcher stated that one
of the symptoms which separate the bipolar child from the
child was that the bipolar child exhibited mood changes.
To me this was a typical way of fitting the definition to
of criteria. By definition, the bipolar child exhibits mood
changes because the researcher says it does.
Over the years, I have observed children who were labeled
Hyperactive, ADD (now ADHD), Autistic, and Bipolar. Years
ago I believed
that each one of these so-defined conditions were external
manifestations of impaired brain chemistry (for-want-of-a-better-term).
What, perhaps, distinguished the different outward clinical
manifestations were: 1) what particular part or region of
the brain was affected, 2) the exact chemical nature (either
brain chemical deficiency or some toxic element) of the process,
and 3) the degree of involvement, either more than one part
or region involved simultaneously or more than one chemical
deficiency or toxic element).
One child might exhibit dyslexia because the particular region
of the brain involved in spatially relating letters in a
word or sentence is impaired. Another child may exhibit antisocial
behavior in school because that particular region of the
modulating such activity is impaired. What really complicates
the entire interpretation is the situation of dyslexia may
in itself cause the child to question his abilities, he may
feel inadequate, and this entire situation may be a causative
factor in his getting upset and lash out as antisocial behavior,
regardless of any impaired brain chemistry which may or not
Stated differently, any behavior results
from a combination of activities from the brain (as a physical
organ) and from
the mind (as a functioning non-physical thinking entity).
Impaired brain chemistry can cause the physical computer
brain not to
function normally. Additionally, the non-physical mind -
the programmed and programming software - gets into
the act. Do we call Dell who manufactured the computer box
call Microsoft who provided the software?
When viewed in this way, it becomes imperative to fix the
brain problem early before more bad programming situations
increasingly difficult to correct. For unlike a Microsoft
software problem, the human mind is self reprogramming,
is constantly changing and updating.
We believe that the scientific literature
has demonstrated how dietary allergies and sensitivities relate
as causative factors in many dis-ease states. The term allergy
is usually used when we can demonstrate that someone reacts
to an antigen by skin testing or a sample of their serum reacts
in a test tube because the serum contains certain antibodies
which are known to mediate the allergic response. Sensitivities
may relate to other factors which cause someone to react to
their environment. Allergies and sensitivities can result from
exposure to foods (milk, eggs, wheat, etc.), inhalant allergens
(animal danders and pollens), toxins (smoke, odors, fumes),
and contact-type irritants (poison ivy and oak).
Stated in another way, sensitivity is a more general term
encompassing reactions which are classified as true immediate-type
(Ig E antibody-mediated sensitivity), delayed-type allergy
(cell-mediated) and the non-antibody, non-cell-mediated
sensitivities which include the toxic, enzyme-lacking,
and metabolic sensitivities
TABLE I: TYPES OF SENSITIVITIES
- Antibody-mediated: immediate-type reaction, mediated through
Ig E class of antibodies; reaction occurring usually within
one to four hours after challenge; true allergy by definition;
conventional allergy test (RAST, cytotoxic) positive; skin
tests, if performed properly, can be useful; direct challenge
- Cell-mediated; delayed-type reaction, mediated through
mononuclear lymphoid cells; reaction occurring 24 to 48 hours
after challenge; may be called delayed allergy; conventional
allergy test negative, except for skin tests which some now
believe are useful; direct challenge test positive.
- Non-antibody, non cell-mediated, sensitivity not falling
in types 1 and 2; can be immediate or delayed; conventional
allergy tests negative; direct challenge test positive. Subtypes
- Toxic Example: sensitivity to nightshade solanine
- Enzyme-lacking Example: lactose intolerance; "sloppy" enzyme
in Methyl Malonic Aciduria and in subsequent schizophrenic
population deficient in serotonin (a brain chemical mediator).
- Metabolic Example: sensitivity to sugar and caffeine.
Many conventional trained allergists may take issue with our
concepts and approach. There are, however, many avante-garde
allergists and nutritionists, such as Doris J. Rapp and Dr.
Jeffrey Bland who have had the courage to write of their clinical
experience even in the face of criticism from some of their
peers. What makes these progressive allergists correct is the
fact that their approach has solved clinical problems not solved
by previously held concepts.
TABLE II: POSSIBLE SYMPTOMS OF ALLERGY AND SENSITIVITY
A. Organ Involvement (Symptoms)
- Skin acute: itching, rash, hives, edema, excessive perspiration.
- chronic: eczema, psoriasis, acne.
- Gastro/acute: Bellyaches, nausea, vomiting, upset stomach,
bloating, bad breath, gassy stomach, belching, diarrhea,
- Intestinal chronic: Colitis, Crohnís disease.
- Kidney and acute: Itching and burning on urination, need
to rush to urinate, wetting
- bladder pants in daytime or in bed.
- chronic: Possibly nephrotic hypertension.
- Respiratory acute: wheezing, asthma, year-round stuffiness,
watery nose, sneezing,
- tract nose-rubbing, increased production of mucus resulting
in increased risk of upper and lower respiratory infections.
- chronic: Emphysema.
- Ear acute: ringing in ears, dizziness.
- chronic: repeated formation of fluid behind eardrums and
chronic middle ear infections.
- Joints acute: general aches and pains.
- chronic: arthritis.
- Muscles acute: aches in back, neck and other muscles,ígrowing
pains,í or pain and aches unrelated to exercise.
- Lymphatic acute: swelling of lymph nodes of neck
- system and chronic: edema of legs. chronic: glands
- Face acute: pale, dark eye circles, puffiness below eyes.
- Eyes acute: red and itchy eyes. chronic: glaucoma.
- Head and acute and chronic: head-aches, sinusitis.
- chronic: sinuses
- Brain see Cerebral Allergy (Part B)
B. Cerebral Allergy (Symptoms)
- Allergic - Tension-Fatigue-Syndrome (Nervous System Symptoms).
Hyperactive, wild, unrestrained, delinquency. Talkative (explosive,
stuttering, constant). Dyslexia and other reading problems.
Inattentive, disruptive, impulsive. Short attention span,
learning disabilities, difficulty concentrating, poor memory.
Restless legs, finger tapping. Clumsiness incoordination,
tremor. Insomnia, nightmares, inability to fall asleep. Nervous,
irritable, upset, short-tempered, anger, fear. High strung,
excitable, agitated, emotional instability. Moody, tired,
weak, weary, exhausted, listless, depressed. Easily moved
to tears, easily hurt. Highly sensitive to odor, light, sound,
pain, and cold.
- Other Symptoms:
- Manic-depressive states
- Childhood autism
TABLE III: SYMPTOMS OF EARLY VITAMIN DEFICIENCY
- B1 (Thiamine)
Loss of appetite, depression, irritability, confusion,
loss of memory, inability to concentrate, sensitivity
- B3 (Niacin)
Anxiety, depression, fatigue, hyperactivity, headache,
insomnia, hyperesthesia (increased sensitivity to touch).
Later symptoms include: failing vision, hypersensitivity
to light and odors, dizziness, dulled sense of taste
- B6 (Pyridoxine)
No specific symptoms. This vitamin is a precursor for
at least 50 enzymes necessary for normal body function.
It is also required for zinc utilization.
- B12 (Cyanocobalamine)
Depression, agitation and hallucinations.
- Panthothenic acid
Irritability, depression, tension, numbness, dizziness,
and a sullen disposition. This vitamin is needed to respond
- C (Ascorbic acid)
Listlessness and blood vessel problems. Rats need three
times as mich vitamin C when stressed. Humans apparently
also require additional vitamin C for mental and physical
The incidence of kidney stones has nearly
doubled both in the United States and Great Britain during
the past 20 years. It is estimated that one out of every 15
men int eh United States has calcium oxalate kidney stones.
It appears to be half that rate in women. Admittedly, many
of these individuals do not seek medical attention because
their disease is subclinical, probably due to the fact that
the stones are very small and pass as gravel in the urine.
If an individual develops symptomatic kidney stone, he has
a 50/50 chance of developing another one. The chance of recurrence
in a given year is eight to ten percent.
The severity of the disease can vary from being subclinical
where the stones are very small and pass with the urine unnoticed
by the individual, to being clinically associated with tremendous
pain and suffering in the case of larger stones. Blockage
of the urinary tract by stones can lead to back up of urine
kidney destruction. The cost of medical care for this condition
has been estimated to be $50 million during the single year
of 1978. It is considerably more now.
Considering the fact that kidney stones do not occur in populations
still eating basic native unrefined foods, we might ask why
its incidence has increased so much in Western countries
whose dietary habits are quite different? The kidney filter
from the body metabolic waste products, and the urine reflects
what we consume as food and our metabolism.
Nutritional therapy should be instituted not only to cure
milder forms of kidney stones but also prevent their formation
Philosophical comment: Both calcium and oxalate (and also
phosphate) are normal constituents of the body and are excreted
urine. Calcium, of course, is ingested as an ingredient of
food. Oxalate is also found in some food. Some authorities
restrict oxalate-containing foods in individuals prone to
develop kidney stones. But oxalate is also manufactured by
two different compounds: ascorbic acid (vitamin C derived
from foods and supplements) and glyoxalate (a breakdown product
of certain amino acids, including glycine and serine).
The philosophical question to ask is why does the presence
of two natural and normal substances ñ calcium and oxalate ñ produce
kidney stones in some individuals while others are able to
handle them without adverse effect? Could it be that some
individuals are lacking some nutrient(s) required by the
body to successfully
metabolize these substances.
Types of stones. It is generally agreed that the most prevalent
kidney stones contain calcium oxalate, as high as 75% in
some surveys. To a lesser extent, stones are composed of
phosphate. Some contain a combination of calcium oxalate
Cystine stones and uric acid stones are occasionally observed,
but these are not as common as the ones already mentioned.
From the responses to nutritional therapy, the following risk
factors have been identified:
- Excess calcium and/or magnesium deficiency
- Excess oxalate ingestion
- Vitamin B6 (pyridoxine) deficiency
- Glutamic acid and/or lysine deficiency
- Vitamin C (ascorbic acid) deficiency
- Vitamin A deficiency
- Excess refined carbohydrates
- Intestinal resection
- Heavy meat diet
There is considerable
evidence showing a causative relationship of kidney stones
with dietary imbalances and vitamin deficiencies. Prevention
and therapy would, of course, be structured around these consideration.
is diabetic neuropathy?
Diabetic neuropathy, a nerve disorder caused by diabetes,
is characterized by a loss or reduction of sensation in the
feet, and in some cases the hands, and pain and weakness in
the feet. The symptoms of diabetic neuropathy vary among patients.
They may be slight at first with some mild cases going unnoticed
for a long time.
The first sign of the disease is usually numbness, pain, or
tingling in the hands, feet, or legs. After several months
or years, this may lead to weakness in the muscles of the
feet. Occasionally, some may experience foot drop, a condition
which causes individuals to trip over small things such as
door thresholds. Occasionally, diabetic neuropathy can flare
up suddenly and affect a specific nerve that may result in
double vision or drooping of the eyelid, or weakness and atrophy
of the thigh muscles. Nerve damage caused by diabetes generally
occurs over a period of years and may lead to problems with
internal organs including the digestive tract and sexual organs.
These problems can then tend to cause indigestion, diarrhea
or constipation, dizziness, bladder infections, and impotence.
The loss of sensation in the feet is important as it may increase
the possibility of injuries of which the patient is not aware.
These foot injuries can develop into ulcers or lesions that
can become infected. In some cases, ulcers may not heal and
amputation may be required.
What causes diabetic neuropathy?
Nerve damage occurs in people who have had diabetes because
their blood sugar level is higher than normal. Over time,
high blood sugar levels damage the blood vessels and nerves.
This is why people who do not control (or cannot control)
their blood sugar very well seem more likely to develop diabetic
neuropathy. Men have diabetic neuropathy more often than women.
How do I know if I have diabetic neuropathy?
If you have numbness in your feet and toes, you may have diabetic
neuropathy. You may notice that cuts and sores on your feet
do not hurt as much as you would expect them to. The following
are also symptoms of diabetic neuropathy:
Pain or burning feeling in your legs; foot drop as mentioned
A feeling of lightheadedness that causes you to fall;
Diarrhea and constipation;
Failure to get an erection (in men).
What will happen if the nerves in my legs and feet are damaged?
If diabetic neuropathy has damaged the nerves in your legs
and feet, you may not be able to feel pain in those parts
of your body. This is a problem because pain can be a useful
signal. If you have no feeling in your feet, you could have
an injury and not know it. In addition, your muscles might
atrophy (lose mass and decrease in size), causing yo to have
trouble walking. The skin on your feet might crack and develop
sores. If the sores get worse and become infected, you might
have to go to the hospital, or possibly have your foot amputated.
Because diabetes makes it harder for an injury to heal, it
is important to take especially good care of your feet.
What can I do to avoid diabetic neuropathy?
Most importantly, keep your blood sugar under control. Perhaps
it is time to start injectable insulin. The testing methods
and devices have been simplified considerably, and taking
insulin twice a day can become so routine that you will hardly
Eat a variety of foods and begin eating a good diet avoiding
especially refined sugars and carbohydrates. If you are overweight,
lose weight by starting something like an Atkins’s Diet
initially. If you have not exercised in a while or you have
other health problems, talk with your nutritionally minded
physician before starting an exercise program. Start slowly
and work up to exercising 4 to 6 times a week for 30 to 60
minutes at a time.
If you already have diabetic neuropathy, exercising may be
difficult, but in time, as your condition improves, you may
Can diabetic neuropathy be treated and cured?
Yes it can. Unfortunately, conventional physicians are ignorant
of the great strides made by nutritionists in treating diabetic
neuropathy. But nutritionally minded physicians can guide
you in an extensive supplementation program including vitamins,
minerals, and enzymes. The aim of nutritional treatment is
Change the lipid (fat) characteristics of blood corpuscles
to make them deformable;
Induce angiogenesis: regenerate the capillaries thus obviating
the consequences of continuing neural hypoxia (low oxygen);
Encourage nerve growth;
Increase the overall oqygen-delivery capacity of the blood
Recovery is usually slow, but in due time – a period
of one to two months to begin to experience a beneficial response
to 6 to 8 months to experience a 95% cure rate. The following
case in point illustrates what can be expected:
A 68 year old man, a physician, who had let his diabetes get
seriously out of control was beginning to experience foot
drop. He began to trip over small things such as door thresholds.
Being a medical man, he should have noticed signs of foot
drop, but as is usually the case, a person too close to a
problem may sometime miss the obvious.
While in Russia, he ran from a parking lot to the airport
bank to exchange some money. As he tried to jump over a small
chain barrier, no higher than 4 inches high, he fell flat
on his face on to the cement pavement. As he pulled himself
up with bruises on his face and knee, it dawned upon him what
was happening. He exclaimed: “I have foot drop.”
He then started to put it all together.
Over the next month, his condition worsened tremendously.
Soon he was unable to climb or go down stairs easily, and
he was literally unable to walk without the assistance of
a cane. He experience numbness and tingling, especially in
his right leg, and to make things worse, he was having extreme
difficulty with pain in the right knee which he injured in
He was placed on insulin to get his diabetes under control,
and he began to adhere to a good diet, avoiding refined sugar,
carbohydrates, milk and dairy, and wheat products. He was
placed on an extensive supplementation program and within
three weeks started to experience improvement. He was able
to shed the cane within 6 weeks but still having considerable
difficulty going up and down stairs. Within 4 to 5 months
he was over 95% improved. The muscle mass of his right leg
which had atrophied considerably because of relative disuse
started to increase in size and he was able to maneuver steps
Important to note is that conventional medicine has no good
cure for diabetic neuropathy.