parzival-therapies

Autism

Mon, 01 Feb 2021 16:33:48 GMT

A Family’s Experience of HANDLE

by Belinda Nunn

George never crawled and took his first wobbly steps at the age of two and a half; he has only recently crawled up the stairs. His fine motor skills are less developed than my sister’s ten month old son, and he still explores everything orally. George appears to feel little or no pain, and he barely reacts when he drops heavy objects on his toes, or slams a finger in the door.

I was fascinated. Did this mean that there could be other areas I could support that would in turn help George with his motor skills? I immediately got onto the website and signed up for a free introductory lecture being held locally and ordered a copy of ‘The Fabric of Autism’. The book’s author, Judith Bluestone is the founder of The HANDLE Institute, and was herself challenged by autism as a child.

George was given a sensory diet from his OT, but he would avoid many of the activities and I felt uncomfortable pushing him to take part. His motivation to try new toys or games was so low, he would lose interest quickly as he was more conscious than anyone of his body’s limitations. I was becoming frustrated by not being able to help him and again uncomfortable as I coaxed him into trying to push, or turn toys in an effort to awaken the sensitivity in his fingers. It was while discussing these challenges with another Son -Rise mum that I first heard of HANDLE® Therapy. She explained to me that whilst her son had championed many of the challenges autism brings (so much so that he has recently started mainstream school) he was still unable to hold a pen. After working with a HANDLE practitioner, and strengthening the binocularity of his eyes he was now holding a pen and beginning to write. It wasn’t that he didn’t want to hold a pen; he avoided it because he couldn’t focus his eyes adequately enough to be able to hold a pen. I couldn’t put the book down and, if you haven’t already, I urge you to read it. I was fascinated, intrigued, overwhelmed and deeply moved by what I was reading. As Bluestone describes her experiences and how she helped herself through them I was again reminded of how brave and courageous our children truly are. She eloquently explains how the repetitious and exclusive behaviors our children exhibit are direct clues as to which systems need strengthening, and that they are doing the best thing for themselves at that time to alleviate the symptoms they are experiencing.

My husband and I had already chosen not to try and prevent George from “isiming” or “stimming”, and this in turn led us to The Son-Rise Program.

We and George’s volunteers join him in these behaviors as a way to understand what he is experiencing, to create a rapport; and to build trust. Through joining him we have realized that his “isms” have a therapeutic effect for him, but after reading Bluestone’s book and attending the lecture I was being shown that these behaviors bore a direct link to specific physiological systems that were compromised. I signed up for an Introductory Course in HANDLE Therapy given by Sean Williams. It was fascinating, easy to follow, fun and importantly inexpensive! Here I learned that simple activities could strengthen compromised systems and in turn help others to function effectively. All the information was substantiated by anatomy and physiology.

Convinced this could help George, I booked an assessment with Sean Williams. After completing a detailed HANDLE questionnaire covering history, health, diet, behavior, etc, we went for George’s HANDLE assessment. It was a truly enjoyable three hours!

I don’t believe our children can be assessed in half an hour. At last here was someone in no rush, letting George take the time he needed to settle, adjust and relax in a new environment. Sean began by asking George what he would like help with and I replied! “Hey, I’m asking George! I’ve got lots of questions for you later!”, replied Sean! George quickly and easily responded to Sean’s respectful, calm and patient nature and was soon bringing him toys and happily playing with him. That was the assessment! Obviously Sean was

constantly observing and the session was DVD recorded for reflection and we were given a copy too. I sat back and enjoyed watching them together feeling relaxed and immensely proud of my son.

Other assessments have left me feeling despondent and hopeless We saw Sean a couple of days later for a presentation of what Sean had seen as areas to concentrate on and possible activities to help strengthen them. For George, the prime concern was the vestibular system, his proprioception and his autonomic nervous system. Sean explained that until these roots had taken hold the trunk could not grow, nor the branches, and least of all the fruits. Sean gently introduced the simple activities to George, and patiently taught me how to do them. George becomes the teacher as I allow him to show me when he has had enough, and by reading his subtle ‘changes of state’. George directs how much or how little, how strong or how softly. Sean amazed me as he often remarked: “See that George curled his toes? That’s enough for you, isn’t it George”. It was like watching a ‘horse whisperer’ and I soon discovered that my son was far more sensitive than I had thought! We left with ten activities specifically modified for George, and so began our HANDLE Program.

He is less wobbly, far more grounded and steady on his feet. He is also avoiding obstacles in his path. If he does fall he has begun to touch the area he just bumped. He is using both hands together when playing with toys or holding objects, instead of grabbing mine as a prop. He is chewing his food more satisfactorily. There is plenty of room for improvement, believe me, but it’s a start. And the greatest thing is that George appears to be far more confident in his body.

Last week he ran into the garden, climbed the frame, sat down and slid down all by himself. He has never done that before! The activities have evolved into our personal games together. George now recognizes them and even offers his toes, or hands in anticipation. The activities have flowed easily into his Son-Rise Program and I look forward and enjoy doing them. We have monthly check-ups with Sean to see how George is progressing and to help me be as effective as I can. The activities are always reviewed and modified or replaced depending on how George accepts them.

Over the last two months we have seen great changes that have been gradually emerging almost without us noticing. George is calmer and he spends far less time running back and forth saying “Eeeeeeeee”. At bedtime he now winds down peacefully. It’s as if he has learned how to relax. He is falling asleep in less than thirty minutes and staying in his bed. It used to take him hours!

I thoroughly recommend getting your child seen by a HANDLE Practitioner. I have learned so much more about my son from the past two months and continue to do so. It has been an enjoyable, stress-free process for us and more importantly for George. It is relatively inexpensive considering the amount of time a Practitioner spends with a child and the work involved in putting a program together. Best of all, it’s helping George and it’s empowering for me and my husband to have another way to help and bond with our beautiful boy.

Needs to Fidget

Mon, 01 Feb 2021 16:20:19 GMT

The Sensory Motor Cortex

Take a look at the drawing in the upper left corner. Note that there is a little “man” lying across the motor cortex (in red). Further note that his hand and his lips are HUGE. This is to represent how much of the brain deals with information from the hand and mouth in the sensory cortex (blue), and how much of the brain is used to send information to the hand and mouth from the motor cortex.

This means that motor activity, performed by the hand or the mouth, requires neural activity in a very large area of the brain. Likewise, any sensory input to the hand or mouth stimulates a very large area of the brain.

When we stimulate large areas of the motor and sensory cortex through fidgeting, we are helping ourselves to stay alert, centered, and focused. Additionally, since the nerve centers for the hand and mouth are positioned right next to one another in both the sensory and motor cortex, when one is stimulated, the other is also stimulated (determined through neurosurgical research). Move your hand and the oral (mouth) area of your cortex is stimulated. Or move your mouth and the area related to your hands is stimulated. Hence, one of the reasons people move their hands so much when they are talking!

Surrounding the motor and sensory cortex you will see the words “speech” and “hearing,” depicting speech and hearing centers in the brain. As we fidget, our nerve pathways are “reaching out” and connecting to the speech and hearing centers.

Aren’t we wonderfully mapped? Next time you feel inclined to tell someone to stop fidgeting, think about how much of his or her brain you will be turning off!

PEOPLE SHOW US WHAT THEY NEED:

Playing with: hair, toys, pens, pencils, erasers, worry beads, coins in a pocket, jewelry Fingering: satin edges of blanket, fur, silk, corduroy, rosary beads, a stone

Chewing on: gum, clothing, jewelry, fingers, nails, toothpicks, pencils, pens, toys Curling the edges of papers or napkins

Doodling while talking on the phone or listening to a lecture Tapping fingers, picking at fingers/nails, pulling on lips,

Putting fingers and hands around the mouth

Sit Still and Listen

Thu, 07 Nov 2019 13:57:40 GMT

“Sit Still and Listen”

from Turning Points: Pivotal Insights into Behavior and Learning

by Judith Bluestone, Founder of The HANDLE Institute Seattle, WA

Condensed with permission of the author by Rita R. Pearson, Certified HANDLE Screener, Bend, OR

For some children, “Sit still and listen” are two contradictory statements. For the child who needs movement to keep her vestibular* system alert, and thus energized so she can listen, following the direction to sit still means tuning out and missing the learning that is taking place.

In the classroom, this student might be observed stretching, yawning, pushing off from the table, bouncing her head around, rocking from side to side in her chair, getting up and jumping from time to time, or engaging in other fast and sudden movements. She is not trying to be distracting or showing boredom, but is compensating so she can focus on the auditory or visual demands of learning. She knows what the teacher wants and that it’s important that she listen, so she moves and bounces to keep her vestibular system alert and energized so she can listen.

Other symptoms might include motion sickness, avoidance of carnival rides, merry-go-rounds, and swings. Even watching things move might cause dizziness or nausea. Difficulty reading or writing in cursive might occur because of the circular movement. Another child will use excessive movement to dull vestibular feedback to avoid feeling overwhelmed, by spinning himself or watching things spin, but doesn’t get dizzy or nauseous.

These children’s behaviors are often seen as disruptive or defiant when they are actually self-protective, which is why behavior modification isn’t effective. Drug therapies mask or plug behaviors, with the risk of different or more violent behaviors emerging later on, because the underlying problems have not been dealt with.

The HANDLE ^® Institute provides a non-drug approach that looks for root causes behind learning and behavioral challenges that make daily life difficult. Using simple activities to strengthen those areas of the nervous system that are found to be weak or are not connecting with other areas of the nervous system, doors are opened to academic, behavioral, social, professional, and vocational success.

*Vestibular System, in simplified terms, is the inner ear. It’s combined perceptions give us three dimensional organization in space, telling us where we are, what we’re hearing, what we’re seeing, and how we’re going to respond. Stimulation of the system is induced not only by sound, but more significantly by movement (in particular rotational movement), responses to gravity, and altered kinesthetic states. Directly or indirectly it is responsible for nearly all of our motor functions and some of our sensory functions.

Truth About Blood Sugar

Thu, 25 Feb 2016 13:52:47 GMT

It is widely held that the primary instigator of diabetes is sugar, which has led to recommendations to eat a low carbohydrate diet and avoid sugar at all costs, including fruit. Sugar and unhealthy carbohydrates from things like pastries, cakes, cookies, doughnuts, and candy are indeed bad for us and should be avoided. However, our bodies need healthy carbohydrates to function, which can be found in foods such as butternut squash, sweet potatoes, carrots, lentils, black beans, berries, apples, and other fruits.

When we eat carbohydrates (regardless of the source), our body breaks them down into glucose (blood sugar), which becomes the fuel that keeps us going—and keeps us alive. When glucose levels rise, our pancreas secretes the hormone insulin. Insulin helps usher glucose out of the bloodstream and into our cells where it can be used for energy, and keeps our blood sugar levels stable. However, this process can go awry if the pancreas fails to produce enough insulin, or if some of your cells stop responding to insulin, which is called insulin resistance. In either case, blood sugar levels remain elevated, putting you at risk for type 2 diabetes.

The Role of Fat

Contrary to popular belief, one factor that is much more likely to put you at risk for insulin resistance and diabetes than healthy carbs such as those listed above is a high-fat diet. There are several reasons for this. First, high blood fat levels put a major strain on your liver, pancreas, and adrenal glands, which work together to manage your blood sugar levels. Your liver has to shoulder the burden of processing the fat you eat, so a high-fat diet can make the liver sluggish and unable to store and release glucose as it should. Excess fat burdens your pancreas because it needs to release enzymes to aid fat digestion.

Additionally, when blood fat levels are high, the adrenals flood the body with adrenaline. While this increases digestive strength to help move fat through your system, excess adrenaline can wear away at the pancreas, reducing its ability to produce enough insulin to keep your glucose levels in check. Lastly, high blood fat levels can prevent glucose from entering cells. This is not to say that all fat, even healthy fats such as nuts, seeds, and avocados, are bad for us and need to be completely eliminated.

Regardless of your chosen diet, fat intake just needs to be moderated to avoid excessively high blood fat levels when you are dealing with prediabetes or type 2 diabetes. For instance, if you eat a vegan diet, reduce the amount of fat you take in from nuts, nut butters, seeds, oils, avocados, etc. If you are ovo-lacto vegetarian, cut back on eggs, dairy, nuts, seeds, oils, avocado, etc. If your diet includes animal protein, cut back to one serving of meat per day (even lean meats contain appreciable amounts of fat).

Scaling back on fat in this manner helps ease the burden on your pancreas, liver, and adrenal glands, which goes a long way toward preventing and/or healing from diabetes. If you opt to maintain a high-fat diet (which may normalize your A1C levels in the short-term), it becomes especially important to limit your carb intake, as a diet high in both fat and carbs will tax your bodily systems that much more. Ultimately, reducing dietary fat and including healthy carbs of the kind listed above will help give you the best shot at healing from diabetes and help keep your A1C levels in a healthy range on a more permanent basis.

The Role of Adrenaline

A precursor to type 2 diabetes is hypoglycemia (when glucose levels drop below normal), which is due to a stagnant, sluggish, overburdened, or weakened liver and dysfunctional adrenal glands. In fact, both type 2 diabetes and hypoglycemia typically begin with malfunctioning adrenals. When you experience chronic stress, for example, your adrenal glands secrete copious amounts of adrenaline, which is very damaging to the pancreas. Hypoglycemia can also occur if you don’t eat at least a light, balanced snack—e.g., a fruit (for sugar and potassium) and a vegetable (for sodium)—every two hours.

Skipping meals forces your body to use up your liver’s glucose storage, driving the body to run on adrenaline, which can damage your pancreas and lead to insulin resistance. Too little adrenaline can also impair your pancreas, as it forces it to work overtime to compensate. Adrenal fatigue, in which unstable adrenals alternate between producing too much and too little adrenaline, can also harm your pancreas as it tries to compensate for dry spells of adrenaline and then gets scorched by floods of it.

Healing Foods

In addition to scaling back fat intake, it is important to incorporate healthy carbohydrates into your diet. Healing carbohydrates such as squash, sweet potatoes, other root vegetables and fruit contain critical nutrients for optimal health, and when the natural sugars in these healthy carbs are bonded to these nutrients, it does not wreak havoc on your blood sugar levels the way processed sugar does.

Wild blueberries, papayas, blackberries, apples, and raspberries are top fruits to eat if you have type 2 diabetes or hypoglycemia. Vegetables to focus on include spinach, celery, sprouts, kale, and asparagus. These foods help detoxify the liver, strengthen glucose levels, support the pancreas, boost the adrenal glands, and stabilize insulin. To keep your blood fat in check, it is best to avoid cheese, milk, cream, butter, eggs, processed oils, and all sugars except for raw honey and fruit.

While these recommendations fly in the face of conventional strategies for preventing and managing type 2 diabetes, emphasizing nutrient-dense fruits and vegetables and reducing dietary fat eases the burden on your liver, pancreas, and adrenals, helping ensure that they can perform their duties, including keeping your blood sugar as stable as possible. Make friends with healthy carbs and fruit, curtail your fat intake, and reclaim the healthy life you are meant to live!

Listen to the radio show above to learn more about the true causes of both type 1 and type 2 diabetes. You can also learn more about how to address type 2 diabetes and hypoglycemia in Anthony William’s book Medical Medium: Secrets Behind Chronic and Mystery Illness and How to Finally Heal .

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Heavy Metal Toxicity

Wed, 21 Nov 2012 13:52:47 GMT

THE MOST COMMON HEAVY METALS, THEIR SOURCES AND THEIR EFFECTS

Published on November 21, 2012

Below is a summary of the most common heavy metals, their sources and the burden they add to the human body as provided by Doctor’s Data Inc . Doctor’s Data Inc (DDI) is a premier clinical laboratory with over 30 years experience that specializes in essential and toxic elemental testing. Their tests are utilized to detect, asses, prevent and treat heavy metal burden in humans, as well as nutritional deficiencies, gastrointestinal function, hepatic detoxification, metabolic abnormalities, and diseases of environmental origin.

COMMON HEAVY METALS:

ALUMINUM

Common sources of bioavailable Aluminum include: aluminum cookware, flatware and especially coffee pots; aluminum hydroxide anti-acid formulations; some types of cosmetics, especially deodorants; and some herbs or herbal products. Aluminum cookware is particularly of concern if acid foods are cooked such as tomato paste (contains salicylates). In cosmetics and deodorants, aluminum chloride may be present as an astringent. In water purification, alum (sodium aluminum sulfate) may be used to coagulate dispersed solids and improve water clarity. Alumina or Al203 is very stable chemically and not bioavailable. Silica limits the solubility of aluminum and aluminum silicate is not very bioavailable. Clays, bentonite for example, contain aluminum that has poor bio-availability. Aluminum food containers are manufactured with polymer or plastic coatings that prevent direct food-aluminum contact provided such coatings are not damaged. In the GI tract, phosphates react with aluminum ions forming insoluble aluminum phosphates. If this phosphate-blocking were 100% efficient, then virtually no aluminum would be absorbed. Evidently, this phosphate-forming process is incomplete because body tissue levels (such as hair) usually contain measurable amounts of aluminum. In the body aluminum follows a path of increasing phosphate concentration: plasma, cytosol, cell nucleus. Once in the nucleus, it adversely affects protein formation. Long lived cells such as neurons are susceptible to long-term accumulation. Aluminum is considered neurotoxic and is implicated as a stabilizing agent (via aluminum phosphate bonds) in neurofibrillary tangles in Alzheimer’s disease (Science, 267, pp 793-4, 1995). In cells, Aluminum inhibits the citric acid cycle enzyme isocitrate dehydrogenase which catalyzes formation of alpha-ketoglutaric acid. An effect of this inhibition could be hyperammonemia. Aluminum also inhibits hexokinase, a magnesium dependent phosphorylating enzyme. Without intervention, Aluminum accumulates continually in the body with the highest concentration occurring at old age or death. Fatigue, hypophosphatemia, increased prothrombin time, and porphyria are consistent with Aluminum excess. A hair element test can be used to corroborate increased body burden of Aluminum. An oral provocation with the amino acid glycine, 80 mg/Kg body weight (in divided doses) 24 hours before a diagnostic EDTA chelation with subsequent urine collection can be done to confirm Aluminum excess.(Eliminate food/beverage sources of Aluminum during this procedure.)

BIBLIOGRAPHY FOR ALUMINUM
1. Ganrot P.O. “Metabolism and Possible Health Effects of Aluminum”, Environ. Health Perspectives, 65, pp. 363-441 1986.
2. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans , Lewis PubI, Chelsea Ml pp 16-20 1986.
3. Lukiw W.J. “Aluminum and the Nucleus of Nerve Cells”; Brenner S. “Aluminum, Hot Water Tanks and Neurobiology”; Jackson J.A. “Aluminum from a Coffee Pot”; 3 letters all on pages 781-82 of Lancet,April 8, 1989.
4. Fulton B. and E.H. Jeffery, “Absorption and Retention from Drinking Water”, Fund. & AppI. Toxicology 14 pp 788-96 1980.
5. Tsalev D.L. et al. Atomic Absorption Spectrometry in Occupational and Environmental Health Practice vol 1, CRC Press, Boca Raton FL, pp 81-84, 1983.

ANTIMONY

In certain cases when the Antimony levels are higher than expected, the associated symptoms and toxic effects may not be presented. This is because Antimony (chemical symbol Sb) has two valences: Sb+3 and Sb+5. Sb+3 is the more toxic but is mostly excreted in feces. Sb+5, less toxic, binds less well to body tissues and is excreted mostly in urine. Antimony can be assimilated by inhalation of Sb salt or oxide dust, ingested with (contaminated) foods or fluids, or absorbed transdermally. Inhalation may occur in industrial areas where smelting or alloying is done (usually with copper, silver, lead, tin). Sb is present in tobacco at about 0.01% by weight; about 20% of this is typically inhaled by cigarette smoking (Carson et al., Toxicology and Biological Monitoring of Metals in Humans , Lewis Pub. p. 21, 1987). Antimony compounds are used for fireproofing textiles and plastics, and this element may be found in battery electrodes, ceramics and pigments. Antimony can be absorbed with the handling of gun powder or the frequent use of firearms. Recent studies indicate high levels of Antimony in sheepskin bedding produced in New Zealand. Symptoms of mild Antimony contamination may be insidious and multiple including: fatigue, muscle weakness, myopathy, and metallic taste. Chlorides and oxides of both valences of Antimony can be mutagenic and may affect leukocyte function. Antimony can bond to sulfhydryl (-SH) sites on enzymes and interfere with cellular metabolism. Acute symptoms of Antimony contamination include: respiratory tissue irritation and pneumoconiosis with (chronic) inhalation of Antimony dusts, RBC hemolysis with inhalation of stibine (SbH3) vapor, and GI distress if orally ingested. Skin exposure can produce “antimony spots” or rashes which resemble chicken pox. Certain molds can produce the highlyneurotoxic stibine gas from Antimony; stibine inhibits acetylcholinestelase activity. A hair element analysis may be used as a corroborative test for increased body burden of Antimony. Fecal metal analysis can be used to confirm exposure/retention of toxic Sb+3. Antimony may be elevated in urine following administration of DMPS or DMSA.

BIBLIOGRAPHY FOR ANTIMONY
1. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans , Lewis Publishers, Chelsea MI, pp 21-26, 1987.
2. Tsalev D.L. and Z.K. Zaprianov. Atomic Absorption Spectrometry in Occupational and Environmental Health Practice . CRCPress, Boca Raton FL, pp 85-87, 1983.
3. Scriver C.A. et al The Metabolic Basis of Inherited Disease , 6th ed. McGraw-Hill, New York NY, pp 2349-50 on PFK deficiency. 1989.

ARSENIC

Arsenic is a complex metal, that forms a variety of compounds, either inorganic or organic. Organic Arsenic compounds like Arsenobetaine, Arsenocholine, Arsenosugars and Tetramethylarsonium salts contain carbon and are mainly found in sea-living organisms, however occasionally they can be found in species living on land. Inorganic forms of Arsenic, such as Arsenite and Arsenate are generally known to be more toxic and are mainly of geological origin. These can be found in agricultural soil and groundwater used for drinking or irrigation. When the water comes into contact with Arsenic containing minerals or deposits it causes exposure to humans and other life forms mainly through daily ingestion of contaminated food or water. Other ways of Arsenic absorption are through lungs and skin.

Industrially, Arsenic and its compounds are mainly used in the production of pesticides, herbicides and insecticides as well as in semiconductor manufacturing to strengthen copper and lead alloys during batteries manufacturing process. Due to its toxicity to insects, bacteria and fungi, Arsenic is still added to animal food (mainly in US grown industrial poultry and swine production) as a method of growth stimulation and disease prevention. In addition, an estimated of 70% of the world’s Arsenic production is being utilized every year in the preservation of timber used for outdoor products such as residential decks, play structures, fence enclosures or picnic tables. If these products were built before 2004 and have a greenish tinge, there are great changes that they were treated with Arsenic to prevent decay or insect damage. Research has shown that when raining, this Arsenic-based wood preservative leaches from wood and it can be rubbed off from the treated surfaces when in contact with the skin. Children who play on structures or other treated surfaces pick up Arsenic on their hands and later on ingest it when they put their hands in their mouth, rub their eyes or eat. According to Environmental Working Group (EWG) the amount of Arsenic in treated wood can be quite large. For example, a standard 12 foot long 2×6 contains as much as 1 oz. of pure Arsenic that could kill 250 adults. It has been estimated that children ingest 630 µg of Arsenic per playground visit and only 5 minutes hand contact with Arsenic treated wood can add up to 1,260 µg to the current Arsenic load. Even though the US Environmental Protection Agency (EPA) has recently lowered the Arsenic standard in drinking water from 50 ppm (50 µg/liter) to 10 ppm (10 µg/liter), there is still a risk of cancer or other illnesses as the total levels of previous, current and future exposure compound when it comes to one’s body burden.

When the concentration of inorganic Arsenic is measured in urine it shows the absorbed dose of Arsenic on an individual level which typically ranges from 5 to 20 µg Arsenic/liter, but in many instances may even exceed 1000 µg/liter. After entering the body, most toxins do not affect all the organs the same way. Usually, a specific molecular target or organ receives the primary toxic effect and when it comes to Arsenic, the peripheral nervous system is the main target. Early signs of Arsenic exposure are excessive perspiration, muscle tenderness or weakness and changes in the skin pigmentation. According to William A. Croft, medical pathologist and former professor at the University of Wisconsin School of Medicine people with acute exposure to Arsenic could develop associated symptoms and toxic side effects such as intestinal pain, burning eyes and throat, diarrhea, dizziness and/or nausea, sensory loss, cardiovascular failure and even death. Chronic long term exposure or survival of acute exposure can cause loss of peripheral sensory function and loss of central nervous system function, skin pigmentation changes (hyperkeratosis), cancer of the skin and lungs and/or blackfoot disease (BFD), a severe form of peripheral vascular disease (PVD) which leads to gangrenous changes.
Since no levels of Arsenic are considered safe when it comes to exposure to children, signs of Arsenic poisoning for them can be even more severe: loss of speech, seizures, rashes, brain damage, even cancer of the lung, skin or bladder.

Blood, hair, nails and urine biomarker analysis may be used to test for increased body burden of Arsenic. Most of the Arsenic in the blood is bound to red blood cells. When ingested, Arsenic is transformed by the liver to a methylated form of Arsenic and excreted in the urine with a half-life of 3 – 5 days. Since Arsenic is rapidly cleared from blood, this biomarker can only be used in cases of acute Arsenic poisoning or high level exposure. Arsenic is excreted through outer layer of skin and sweat. Arsenic binds to sulfhydryl-containing proteins and concentrates in the hair and fingernails which can be seen as white transversal bands called Mees’ lines.

BIBLIOGRAPHY FOR ARSENIC
1. Gilbert Stephen G., A Small Dose of Toxicology: The Health Effects of Common Chemicals , 1st ed, CRC Press LLC, 2004
2. www.ewg.org

BARIUM

Elevated levels Barium are often observed after exposure to Barium (a contrast agent) during diagnostic medical tests (e.g. “barium swallow”, “upper GI series”, “barium enema”, etc.). Elevated levels of Barium may interfere with calcium metabolism and potassium retention. Acutely high intake of soluble Ba-salts (nitrates, sulfides, chlorides) can be toxic. Chronic exposure to Barium may be manifested by muscular and myocardial stimulation, tingling in the extremities, and loss of tendon reflexes. Due to its high density, Barium is utilized to absorb radiation and is utilized in concrete shields around nuclear reactors and in plaster used to line x-ray rooms. The main use of Barium in medicine is as a contrast medium. Long-term retention of Barium can occur – granuloma of the traverse colon has been reported after diagnostic use of Barium sulfate. Crystalline Barium-titanate is a ceramic compound which is used in capacitors and transducers. Barium is also used to produce pigments in paints and decorative glass. Soluble Barium compounds are highly toxic and may be used as insecticides. Barium-aluminates are utilized for water purification, acceleration of concrete solidification, production of synthetic zeolites, and in the paper and enamel industries. Although Barium is poorly absorbed orally (less than 5%) it can be very high in peanuts and peanut butters (about 3,000 nanograms/gram) as compared to egg, frozen and fast foods such as burgers, fries and hot dogs (400-500 nanograms/gram). It is noteworthy that Barium intake is much higher in children than adults.

Barium levels (as well as the levels other elements) in water can be assessed with water testing as provided by DDI. A conformatory test for elevated Barium is measurement of blood electrolytes as hypokalemia may be associated with elevated Barium.

BISMUTH

This element is considered to be only slightly toxic with ingestion of gram quantities necessary before signs of toxicity occur. Only between 5 and 10% of orally ingested, soluble bismuth salts are absorbed into the blood. Bismuth is a byproduct of lead and copper ore refining. Bismuth has therapeutic uses with antimicrobial, anti-secretory and anti-inflammatory actions. Bismuth subsalicylate (“Pepto-Bismol“) hydrolyzes in the stomach to salicylic acid and insoluble bismuth; it can be effective in halting traveler’s diarrhea. Historically, bismuth was used to treat syphilis. Bismuth is used commercially in low-melting-point alloys and solders and is commonly in “automatic” sprinkler heads for in- building fire protection. Bismuth often is a component of: pigments, paints, glazes for ceramics, glass, and some semiconductor materials. Some cosmetics including lipstick may contain bismuth oxides as a pigment (pearlescent white). Dry cell battery electrodes (cathode) may contain bismuth. At sub-gram quantities, no toxic effects are documented for bismuth. Also, the existence of health problems due to environmental pollution by bismuth is not documented (Tsalev p. 101, 1983). Early physiological signs of bismuth excess may include: constipation or bowel irregularity, foul breath, skin pigmentation changes, and gum pigmentation (blue-black) with stomatitis. Laboratory tests that help to assess bismuth status are whole blood and hair element analyses. Some increase in urine bismuth may follow administration of dithiol chelators (DMPS, DMSA). Bismuth has a very high affinity for sulfhydryl groups.

BIBLIOGRAPHY FOR BISMUTH
1. Harrison’s Principles of Internal Medicine , 13th ed, McGraw Hill, New York, NY pp. 282, 534, 1994.
2. Tsalev D.L. and Z.K. Zaprianov Atomic Absorption Spectrometry in Occupational and Environmental Health Practice CRC Press, Boca Raton FL, pp 101-103, 1983.
3. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans Lewis Publishers, Chelsea Ml pp 44-7, 1987.

CADMIUM

This element is insidiously toxic with chronic accumulations affecting renal function, pulmonary and cardiovascular tissues, bone, and the peripheral nervous system. Without intervention, the biological half-life of Cadmium in humans exceeds 20 years ( Harrison’s Principles of Internal Medicine , 13th ed, pp 2463-64). Chronic manifestations associated with this degree of Cadmium excess include: hypertension, weight loss, microcytic-hypochromic anemia, lymphocytosis, proteinuria with wasting of beta2 microglobulin, emphysema and pulmonary fibrosis (if inhalation was a route of contamination), atherosclerosis, steomalacia and lumbar pain, and peripheral neuropathy. Acute inhalation of Cadmium dusts, fumes or soluble salts may produce cough, pneumonitis and fatigue. Manifestations of Cadmium toxicity may be lessened or delayed by an individual’s protective and detoxication capacities. Zinc and vitamin E are protective; metallothionein and glutathione bind Cadmium and help detoxify itinitially. Smoking can be a source for as much as 0.1 mcg Cadmium per cigarette (HEW Pub. No. NIOSH 76-1 92, US Govt. Printing Ofc., 1976). Some medical authorities consider Cadmium to be a carcinogen for lung cancer ( Harrison’s Principles , 13th ed, op. cit. pp 2463). Other occupational or environmental sources include: mining and smelting activities, pigments and paints, electroplating, electroplated parts (e.g., nuts and bolts), batteries (Ni-Cd), plastics and synthetic rubber, photographic and engraving processes, old drums from some copy machines, photoconductors and photovoltaic cells, and some alloys used in soldering and brazing. “Cadmium Red” as used in dental acrylics (dentures) could be a significant source of exposure for those making dentures or dentists/dental techs making fine- tune adjustments (grinding) to dentures chair side. Cadmium- free acrylic dentures are now available. Depending upon the extent of net retention of Cadmium elevated urine Cadmium may occur after administration of EDTA, and to a much lesser extent DMPS, DMSA, or D-penicillamine. Blood Cadmium measurement may not be indicative ( Harrison’s Principles of Internal Medicine , 13th ed., pp 2463).

BIBLIOGRAPHY FOR CADMIUM
1. Graef J.W. “Cadmium” in Harrison’s Principles of Internal Medicine , 13th ed, Isselbacher et al. eds,McGraw Hill, NY, NY pp 2462-63, 1994.
2. Nat. Inst. Occup. Safety and Health (NIOSH), “Criteria for a Recommended Standard…Occupational Exposure to Cadmium”, H.E.W. Publication No. (NIOSH) 76- 192, 1976.
3. Carson, B.L. et al, Toxicology and Biological Monitoring of Metals in Humans , Lewis Publishers,Chelsea Ml, pp 51-58, 1987.
4. Werbach M.R. Nutritional Influences on Illness 2nd ed., Third Line Press, Tarzana, CA, pp 102,348-49, 643, 679, 1993.
5. Lauwerys R.R. et al. “Cadmium: Exposure Markers as predictors of Nephrotoxic Effects” Clinical Chem. 40 no 7, pp 1391-94, 1994.
6. Whittemere A.S. et al. “Urinary Cadmium and Blood Pressure: Results from the NHANES Il Survey” Environ. Health Persp. 9, pp 133-40, 1991.

LEAD

Sources of lead include: old lead-pigment paints, batteries, industrial smelting and alloying, some types of solders, ayruvedic herbs, some toys and products from China, glazes on (foreign) ceramics, leaded (antiknock compound) fuels, bullets and fishing sinkers, artist paints with lead pigments, and leaded joints in some municipal water systems. Most Lead contamination occurs via oral ingestion of contaminated food or water or by children mouthing or eating Lead- containing substances. The degree of absorption of oral Lead depends upon stomach contents (empty stomach increases uptake) and upon the body’s mineral status. Deficiency of zinc, calcium or iron may increase Lead uptake. Transdermal exposure is slight. Inhalation has decreased significantly with almost universal use of non-leaded automobile fuel. Lead accumulates extensively in bone and inhibits formation of heme and hemoglobin in erythroid precursor cells. Bone Lead is released to soft tissues with bone remodeling that can be accelerated with growth, menopausal hormonal changes and osteoporosis. Lead has physiological and pathological effects on body tissues that may be manifested from relatively low Lead levels up to acutely toxic levels. In children, developmental disorders and behavior problems may occur at relatively low levels: loss of IQ, hearing loss, poor growth. In order of occurrence with increasing lead concentration, the following can occur: impaired vitamin D metabolism, initial effects on erythrocyte and erythroid precursor cell enzymology, increased erythrocyte protoporphyrin, headache, decreased nerve conduction velocity, metallic taste, loss of appetite, constipation, poor hemoglobin synthesis, colic, frank anemia, tremors, nephrotoxic effects with impaired renal excretion of uric acid, neuropathy and encephalopathy. At relatively low levels, Lead can participate in synergistic toxicity with other toxic elements (e.g. cadmium, mercury). Excessive retention of Lead can be assessed by urinalysis after provocation with Ca-EDTA (iv) or oral DMSA. Whole blood analysis can be expected to reflect only recent exposures and does not correlate well with total body burden of Lead.

BIBLIOGRAPHY FOR LEAD
1. ATSDR Toxicological Profile for Lead( 2007 update) http://www.atsdr.cdc.gov/substances/toxsubstance.asp?toxid=22
2. Lead Tech ‘92, “Proceedings and Papers from the Lead Tech ‘92: Solutions for a Nation at Risk” Conference, Sept 30-Oct 2, 1992. Bethesda, MD, IAQ Publications, 4520 East-West Highway, Ste 610, Bethesda, MD, 20814.
3. “ Preventing Lead Poisoning in Young Children “, US Centers for Disease Control, Atlanta, GA, Oct. 1991 Statement, US Dept. of Health and Human Services.
4. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans , Lewis Publishers, Inc., Chelsea, Ml, p. 128-135, 1986.
5. Tsalev D.L. et al. Atomic Absorption Spectrometry in Occupational and Environmental Health Practice Vol 1, CRC Press, BocaRaton, FL 1983.
6. Piomelli S. et al. “Management of Childhood Lead Poisoning”, J. Pediatr 105 (1990) p. 523-32.
7. Shubert J. et al. “Combined Effects in Toxicology – a Rapid Systematic Testing Procedure: Cadmium, Mercury and Lead” – J. Toxicology and Environmental Health, 4:763-776, 1978.

MERCURY

6 grams pure mercury. Diameter of the inner disc: 2 cm.
Source: http://images-of-elements.com

Symptomatology depends on many factors: the chemical form of absorbed Hg and its transport in body tissues, presence of other synergistic toxics (lead, cadmium have such effects), presence of disease that depletes or inactivates lymphocytes or is immunosuppressive, organ levels of xenobiotic chemicals and sulfhydryl-bearing metabolites (e.g. glutathione), and the concentration of protective nutrients, (e.g. zinc, selenium, vitamin E). Early signs of Mercury contamination include: decreased senses of touch, hearing, vision and taste, metallic taste in mouth, fatigue or lack of physical endurance, and increased salivation. Symptoms may progress with moderate or chronic exposure to include: anorexia, numbness and paresthesias, headaches, hypertension, irritability and excitability, and immune suppression, possibly immune dysregulation. Advanced disease processes from Mercury toxicity include: tremors and incoordination, anemia, psychoses, manic behaviors, possibly autoimmune disorders, renal dysfunction or failure. Note that in Mercury contamination of long duration, renal excretion of Mercury (and normal metabolites) may become impaired, and the urine level of Mercury might be only mildly elevated or not elevated at all due to renal failure. Mercury is used in: dental amalgams (50% by weight), explosive detonators; some vaccines in pure liquid form for thermometers, barometers, and laboratory equipment; batteries and electrodes (“calomel”); and in fungicides and pesticides and in the paper industry. The fungicide/pesticide use of Mercury has declined due to environmental concerns, but Mercury residues persist from past use. Emissions from coal fired power plants and hospital/municipal incinerators are significant sources of Mercury pollution. Methylmercury, the common, poisonous form, occurs by methylation in aquatic biota or sediments (both freshwater and ocean sediments). Methylmercury accumulates in aquatic animals and fish and is concentrated up the food chain reaching high concentrations in large fish and predatory birds. Except for fish, the human intake of dietary Mercury is negligible unless the food is contaminated with one of the previously listed forms/sources. A daily diet of fish can cause 1 to 10 micrograms of mercury/day to be ingested; the majority of which is organic, methylmercury. Depending upon body burden and upon type, duration and dosage of detoxifying agents, elevated urine Mercury may occur after administration of: DMPS, DMSA, or D-penicillamine. Mercury accumulation can also be assessed by comparing pre- and post-l.V. vitamin C fecal mercury levels (DDI observations). Blood and especially blood cell analyses are only useful for diagnosing very recent or ongoing organic (methyl) Mercury exposure.

BIBLIOGRAPHY FOR MERCURY
1. Suzuki T. et al eds, Advances in Mercury Toxicology , Plenum Press, New York, 1991.
2. World Health Organization: “Methylmercury” Environ. Health Criteria 101 (1990); “Inorganic Mercury” Environ. Health Criteria 118 (1991) WHO, Geneva, Switzerland.
3. Tsalev D.L. and Z.K. Zaprianov, Atomic Absorption Spectrometry in Occupational and Environmental Health Practice , CRC Press, Boca Raton FL, pp 158-69, 1983.
4. Birke G. et al “Studies on Humans Exposed to Methyl Mercury Through Fish Consumption”, Arch Environ Health 25, 1972 pp 77-91.
5. Pelletier L. “Autoreactive T Cells in Mercury-Induced Autoimmunity”, J. Immunology, 140 no.3 (1988) pp 750-54.
6. Werbach M.R. Nutritional Influences on Illness , 2nd ed, Third Line Press, Tarzana CA, pp 249, 647, 679, 1993.

NICKEL

Pure nickel button, obtained by electrolysis, about 20 grams. Original size in cm: 2 x 2
Source: http://images-of-elements.com

With the exception of specific occupational exposures, most absorbed Nickel comes from food or drink, and intakes can vary by factors exceeding 100 depending upon geographical location, food type, and water supply. Depending upon chemical form and physiological factors, from 1 to 10% of dietary Nickel may be absorbed from the gastrointestinal tract into the blood. Urine reflects recent exposure to nickel and may vary widely in Nickel content from day to day due to the above factors. Sources of Nickel are numerous and include the following:

Cigarettes (2 to 6 mcg Ni per average cigarette)
Diesel exhaust (particulates may contain up to 10 mg/grams
Foods, especially: cocoa, chocolate, soya products, nuts, and hydrogenated oils
Nickel-cadmium batteries
Non precious, semiprecious dental materials
Nickel-containing prostheses
Electroplating, plated objects, costume jewelry
Pigments (usually for ceramics or glass)
Catalyst materials (for hydrogenation processes in the food, petroleum and petrochemical industries)
Arc welding
Nickel refining and metallurgical processes

Most clinically observed Nickel contaminations are manifested as dermatoses – contact dermatitis and atopic dermatitis. However, Nickel hypersensitizes the immune system causing hyperallergenic responses to many different substances. Because Nickel can displace zinc from binding sites on enzymes, it can have inhibiting or activating effects on such enzymes. Nickel sensitivity is observed to be three to five times more frequent in women than in men. Other laboratory tests or clinical findings that would be indicative of nickel excess are; hair element analysis, presentation of multiple allergic sensitivities, dermatitis, positive patch test for “Nickel allergy”, proteinuria, hyperaminoaciduria (by 24-hour urine amino acid analysis). Detoxification treatments with administration of EDTA or sulfhydryl agents (DMPS, DMSA, D-penicillamine) may increase urine Nickel levels depending upon: body burden and mobility in tissues, duration of treatment, dosage and other factors.

BIBLIOGRAPHY FOR NICKEL
1. Tsalev D.L. and Z.K. Zaprianov Atomic Absorption Spectrometry in Occupational and Environmental Health Practice , CRC Press, Boca Raton FL, pp 173-78, 1983.
2. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans , Lewis Publishers, Chelsea Ml, pp 162-67, 1986.
3. Nielsen F.H. in Modern Nutrition in Health and Disease ed. by Shils et al, Lea & Febiger, Philadelphia, PA, pp 279-81, 1994.
4. Medical and Biological Effects of Environmental Pollutants: Nickel, Nat. Acad. Sci, Washington DC, 1975.
5. Ambient Water Quality Criteria for Nickel, US EPA NTIS, Springfield, VA. PubI No. PB81- 117715,1980.

TIN

Ultrapure tin blob. Original size in cm: 3 x 3
Source: http://images-of-elements.com

Ingested tin is not significantly absorbed if it is an inorganic form. Oxide coatings readily form on metallic tin, and salts can quickly oxidize making them insoluble. Organic tin, however, is bioavailable and more readily absorbed. Some organic tin compounds such as short-chain alkyltins can be absorbed transdermally and can cause degeneration of myelin. Food and drink usually provide small daily intakes of (nontoxic) tin, with amounts depending upon type of food, packaging, quality of drinking water and water piping materials. Total daily intake is expected to vary from about 0.1 to 15 milligrams. Tin is present in many metal alloys and solders; bronze, brass and pewter contain the element. Dyes, pigments and bleaching agents often contain tin. Anticorrosion plating of steel and electrical components may also use tin. “Tin cans” are tin-plated steel with a thin outer oxide layer allowing the surface to be shiny but inert. Modern food-containing cans usually haveS polymer coatings that prevent food-metal contact. In the past some toothpastes contained stannous fluoride, a soluble fluoride source for strengthening tooth enamel. Currently most brands of fluoridated toothpastes contain sodium fluoride. Organic tins, the usually toxic forms, are: biocides (triphenyltin and alkyltins) used against rodents, fungi, insects and mites; curing agents for rubbers and silicones (dialkyltin); and methyltin formed bacteriologically (similar to methylmercury). Mildly elevated levels of tin in urine may reflect sporadic dietary intake and excretion; there may be no associated symptoms. A two- or three-fold increase in urine tin levels is not uncommon following administration of EDTA or with sulfhydryl agents (DMSA, D-penicillamine, DMPS). Early signs of chronic organic tin excess can be: reduced sense of smell, headaches, fatigue and muscle aches, ataxia and vertigo. Hyperglycemia and glucosuria are reported. Also, for organic tin exposure, there can be irritation of contacted tissues (eyes, skin, bronchial tubes, or GI tract). Later, immune dysfunction may occur with reduced lymphocytes and leukocytes; mild anemia may occur. A hair element analysis can be used to corroborate tin excess. Tin is commonly elevated in urine from autistic patients following administration of DMSA or DMPS.

BIBLIOGRAPHY FOR TIN
1. Winship K.A. “Toxicity of Tin and Its Compounds”, Adverse Drug Reactions and Acute Poisoning Reviews, 7 no.1, pp 19-38, 1988.
2. Gray B.H. et al. “Inhibition of Tributyltin Mediated Hemolysis by Mercapto Compounds” J. Applied Toxicology 6 no.5 pp 363-70, 1986. Discussed BAL, DMSA, DMPS relative effectiveness in inhibiting a toxic effect of tin.
3. Ganguly B.B. et al “Cytotoxicity of Tin in Human Peripheral Lymphocytes in Vitro” Mutation Research, 282 no.2, pp 61-67, 1992.
4. Tsalev D.L. and Z.K. Zaprianov, Atomic Absorption Spectrometry in Occupational and Environmental Health Practice , vol. 2, CRC Press, Boca Raton, FL, pp 199-204, 1983.
5. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans , Lewis Publ., Chelsea Ml, pp 260-63, 1987.

URANIUM

Depleted uranium (238)
Source: http://images-of-elements.com

Uranium is a radioactive element having 10 isotopes with half lives that exceed one hour. U238 constitutes about 99% of the naturally-occurring uranium. U238 has a half life of 4.5 X 10 to the ninth years. It decays by alpha emission to produce thorium, Th234, the initial step in a decay chain that eventually leads to lead. Alpha, beta and gamma emissions occur during this decay process. Because of the very long half life, the radioactivity danger is only slight. However, exposure to enriched or nuclear fuel grade uranium (high in U235) does pose a health hazard. The major concern for (natural) uranium excess is toxochemical rather than radiochemical. Uranium is a chemically-reactive element, has four valences (3,4,5 or 6), and may combine with: carbonate, phosphate, citrate, pyruvate, matate, lactate, etc. in body tissues. When not excreted in urine, it may accumulate in the kidneys, spleen, liver, and in bone (substituting for calcium in hydroxyapatite). Uranium is nephrotoxic, causing damage to the glomeruli and proximal tubules. An early sign of uranium excess is general fatigue. Renal damage is reflected by proteinuria, hyperaminoaciduria and glucosuria. Albuminuria and urinary catalase are findings consistent with uranium excess. Elevated hair uranium is a confirmatory finding; whole blood and fecal analyses may corroborate recent or ongoing exposures. Uranium is more common than mercury, silver or cadmium in the earth’s rock strata, and may be present, at low levels, in ground (drinking) water. Most commercial use of uranium is for nuclear fuel, but it may be present in ceramics or colored glass, especially ancient or antique, yellow-colored glass.

BIBLIOGRAPHY FOR URANIUM
1. Carson B.L. et al Toxicology and Biological Monitoring of Metals in Humans , Lewis Publishers, Chelsea Ml. pp. 272-75, 1986.
2. Handbook of Chemistry and Physics , 49th ed., CRC, Cleveland, OH, pp B-143-44, 1968.
3. Leggett R.W., “The Behavior and Chemical Assessment of U in the Kidney: a Reassessment”, Health Physics, 57 no.3, pp 365-83, 1989.
4. Byrne A.R. and L. Benedik, “Uranium Content of Blood, Urine and Hair of Exposed and Non Exposed Persons Determined by Radiochemical Neutron Activation Analysis The Science of the Total Environment, 107, pp 143-57 1991.
5. Bentley K.W. and J.H. Wyatt, “Quantitative Determination of Fissionable materials in Human Hair” Environ. Res. 21 pp 407-15, 1980.

Taming Tourette

Sun, 01 Mar 1998 13:52:47 GMT

Taming Tourette's: Family Conquers Disorder with Innovative Treatment

Steve Solimini, who has Tourette's syndrome, uses a hula hoop to develop left and right brain motor skills. Solimini is treating the disorder with a nonmedical approach established by the Seattle- based HANDLE (Holistic Approach to Neurodevelopment and Learning Efficiency) Institute, which advocates exercises to strengthen the neurological system.

Silly String, Crazy Straws and Hula Hoops - these are things Steve Solimini shares with his nephew, Nick Voelker. Solimini, of Fox River Grove, and Voelker, of Cary, don't keep the playthings for fun. The toys are tools to treat Tourette's syndrome.

Solimini and his nephew have the neurobiological disorder that causes involuntary movements and vocal outbursts. These uncontrolled reactions are called tics, which Solimini described. "You actually feel something there, it's like a tingling," he said. "It's like you have and itch, but instead of scratching you want to push on it and hurt it." But with exercises that include bouncing a rubber ball off a wall and writing in pink ink while wearing 3-D glasses, Solimini and Voelker believe they have conquered Tourette's syndrome.

"I can't even remember the last time I had a tic," said Solimini, who lives in Fox River Grove. Voelker smiled at his uncle's words. "[Nick] could never sit still like this," said his mother Terry Voelker.

The program was developed by the institute's founder, Judith Bluestone, based on her 30-year background in the diagnosis and treatment of neurodevelopmental problems.

Bluestone's method identifies the root cause of a client's neurodevelopmental disorder, looking for the underlying stress to the system causing the disorder. Once the stresses have been identified, clinicians develop a program of exercises to strengthen the neurological system. "You ask, 'What does the body normally do to develop the things that aren't working right in that particular individual," Bluestone said.

During his evaluation, Solimini recalled he was asked to put on a pair of red and blue-lens 3-D glasses and describe what he saw.

He saw alternating flashes of blue and red, revealing his eyes were not working in harmony. The exercise of writing in pink ink while wearing 3-D glasses strengthens the optic nerves of the eye looking through the blue lens, he said. Clients are told to stop exercising at the first sign of discomfort or lack of coordination.

Solimini, now a 37-year-old was diagnosed with Tourette's syndrome when he was 13, but the tics started at age 7 when he was in second grade. Classmates mocked him, while the nuns who taught him thought he was misbehaving. Solimini's tics included blinking, clenching his teeth, cracking his neck, snapping his arm out and grunting. He did not explode with profanities, which is a misconception about Tourette syndrome. According to the Tourette Syndrome Association, fewer than 15 percent of people who suffer the disorder will spontaneously curse.

Nick Voelker was diagnosed with Tourette's syndrome and attention deficit disorder when he was in first grade. He started taking the drug Clonidine when he was 6. "Doing homework with Nick was really a trauma," said his father, Ron Voelker. "A 10- minute project turned into 35 minutes of agony."

Despite his medication, Solimini's tics persisted for three decades. "I don't know how I got through the day ticcing," he said. "Not only is it distraction, but it takes so much out of you." Solimini discovered the HANDLE when he found its home page on the Internet (www.handle.org). What he read about the nonmedical approach intrigued him. "It was just different than anything I'd ever looked at," Solimini said. "Just the whole approach to looking at the problem and addressing the problem just made sense." Solimini and his wife flew to Seattle Aug. 4 for treatment.

The HANDLE assessment is conducted in a pair of two- hour sessions, first to evaluate then to present results. Bluestone said clients are asked not to take medication before the evaluation session. "We want to meet the person, not the medication." Solimini was given a 20 minute exercise regimen to follow each morning. When his tics began to subside, he recommended the HANDLE to his sister, Terry Voelker. The Voelkers took Nick to a visiting a HANDLE practitioner in Iowa October 5. One of Nick's exercises was to suck water through a winding Crazy Straw. Despite Solimini's experience, the Voelkers were skeptical when they left the clinic. "We drove home; it was a seven-hour drive," Ron Voelker said, "and it was quiet." But the Voelkers also saw results. Shortly after starting his exercises, Nick ran into the kitchen holding his arms out. He said, "Mom, look how still I can hold my hands."

Nick's grades went up in the last quarter. The Voelkers' minivan now bears a bumper sticker that says "My child is an honor student at Prairie Grove School." "We just can't believe this system of exercises works so well," Ron Voelker said.

It's a success Solimini claims to share. "I'm not just free of Tourette's," he said, "I can think clearer, I'm more methodical."