Hyperactivity or hyperkineses, as the name implies (hyper from the Greek, meaning over and above; active 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 Disorder" (ADHD).

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 ages.

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 motion.

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.

Causative factors:

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 should consider:

• 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.

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 correct. 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 ADD child was that the bipolar child exhibited mood changes. To me this was a typical way of fitting the definition to a set 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 some 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 brain 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 exist.

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 or 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 become increasingly difficult to correct. For unlike a Microsoft software problem, the human mind is self reprogramming, the software 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 allergy (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

1. 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 test positive.
2. 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.
3. 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 include
   1. Toxic Example: sensitivity to nightshade solanine toxin.
   2. Enzyme-lacking Example: lactose intolerance; "sloppy" enzyme in Methyl Malonic Aciduria and in subsequent schizophrenic population deficient in serotonin (a brain chemical mediator).
   3. 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, constipation.
• 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. chronic: acne.
• 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)

1. 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.
2. Other Symptoms:
   • Hallucinations
   • Manic-depressive states
   • Childhood autism
   • Schizophrenia
   • Convulsions

TABLE III: SYMPTOMS OF EARLY VITAMIN DEFICIENCY

• B1 (Thiamine)

  Loss of appetite, depression, irritability, confusion, loss of memory, inability to concentrate, sensitivity to noise.

• 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 and hallucinations.

• 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 to stress

• 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 stress.

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 and 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 and eliminate 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 in the future.

Philosophical comment: Both calcium and oxalate (and also phosphate) are normal constituents of the body and are excreted in the 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 the bodyfrom 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 calcium phosphate. Some contain a combination of calcium oxalate and phosphate.

Cystine stones and uric acid stones are occasionally observed, but these are not as common as the ones already mentioned.

RISK FACTORS

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

SUMMARY

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.

DIABETIC NEUROPATHY

What 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 above;

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 notice it.

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 begin exercising.

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 to:
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 circulatory system.

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 the fall.

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 without difficulty.

Important to note is that conventional medicine has no good cure for diabetic neuropathy.