WEDNESDAY, Oct. 3 (HealthScoutNews) -- British scientists say they have identified the first gene that can be definitively linked to language, offering a glimpse into the genetic basis for the human ability to communicate through speech.

Neurogeneticists at the Wellcome Trust Center for Human Genetics at the University of Oxford say they've identified a mutation on that gene that appears to be responsible for a speech and language disorder called developmental apraxia of speech (DAS), also known as developmental verbal dyspraxia or developmental articulatory dyspraxia.

DAS is a relatively rare disorder characterized by problems with planning and making speech sounds.

Children with the disorder may not make cooing or babbling sounds as infants. They leave sounds out of words, mispronounce vowels and may have problems performing oral movements on command, such as puffing out their cheeks. Words with multiple syllables present the greatest challenge. While speech therapy is somewhat helpful, most children continue to struggle with speech.

"They have articulation problems," says Simon Fisher, co-author of the latest study. "They have problems with using grammar and general sort of language structures." Their comprehension of language is nearly normal, with most of their problems having to do with understanding grammar, but their verbal IQ is slightly lower than average, he says.

For several years, the British Institute of Child Health in London has been studying members of three generations of a family, known as "KE," with DAS.

While the language capabilities of family members were tested and their brains were scanned, not until 1996 had the role of genetics in the disorder been examined. In 1998, the Oxford group reported finding the general location of the suspected genes. Since then, they've been trying to find a specific gene. A report on the discovery appears in the Oct. 4 issue of Nature.

Fisher, a senior postdoctoral scientist, says from the outset, DAS appeared to involve a limited number of genes. "In this case, it looks like there was one gene in this big pedigree causing the problems," says Fisher. "We were able to use fairly straightforward genetic methods to actually focus on it."

The gene, called FOXP2, is located on chromosome 7. In the KE family, a single mutation in the gene disrupts the sequence of a protein that tells other genes to switch on or off.

The researchers say they don't know the exact physiology of the mutation, but previous studies suggest that a region of the brain called the basal ganglia, which is involved in controlling movement, may be subtly different in people with DAS.

The researchers also say they can't tell when the gene mutation occurs. "We're guessing that it's during the development of the embryo, mainly because the family doesn't respond well to speech therapy," says Fisher. "It seems to be present pretty early on in their lives."

Lawrence Shriberg, a professor of communicative disorders and the principal investigator at the Waisman Center's Phonology Project and Clinic at the University of Wisconsin, says the study goes further than ever before in relating a genetic mutation to anatomic structures in the brain. "These genes seem to control the development of the brain, and so the neural structures related to this genetic problem don't develop quite as well," he says.

Shriberg says that this may shed light on whether people with apraxia will, over time, outgrow the problem. "If indeed, some of the brain structures are involved, it calls into question whether the disorder does normalize or not." Clinical studies have not answered the question. "One of the possibilities is that there's not one monolithic disorder, but actually several different types, possibly several different genetic types," says Shriberg. "There's certainly variability in the expression of the disorder within this family," both in terms of severity and test profiles, he says.

Shriberg says because there's no single set of diagnostic markers for this disorder, it's frequently misdiagnosed. It's also difficult to calculate exactly how common apraxia is, although he estimates it affects roughly one to two per 1,000 people. "What's nice about this paper is that it really does point to the direction for better diagnostic classification of children," he says.

However, Fisher cautions, "FOXP2 is not necessarily the master switch. There will be other genes." "This is the first time that we've got an entry point into a process where there may be other genes," he says. "Once we've got one of these genes, we can see what it switches on and off, and presumably, some of those will also be important in speech and language development."

SOURCES: Interviews with Simon E. Fisher, Ph.D., senior postdoctoral scientist, Neurogenetics Group, Wellcome Trust Center for Human Genetics, University of Oxford, England, and Lawrence D. Shriberg, Ph.D., professor emeritus, Department of Communicative Disorders, principal investigator, Phonology Project and Clinic, The Waisman Center, University of Wisconsin, Madison; Oct.4, 2001 Nature
Copyright © 2001 ScoutNews, LLC. All rights reserved.

Study Finds Ear Tubes to be No Help in Development
By Byron Spice and Deborah Mendenhall, Post-Gazette Staff Writers

Doctors implant ear tubes in the eardrums of hundreds of thousands of toddlers each year, but a new study from Children's Hospital has found no evidence to support the common claim that ear tubes help prevent long-term impairment of speech and language development.

The tubes are tiny plastic grommets. When placed in the eardrum, they relieve the pressure caused by fluid that builds up in the middle ear following an infection, a condition called "otitis media with effusion."

But in a study of 429 children with persistent cases of fluid buildup, Dr. Jack L. Paradise and colleagues at Children's Hospital found that it made no difference whether they implanted the tubes as soon as possible or if they waited up to nine months to decide. Either way, the children scored about the same on tests of their speech, language, thinking ability and psychosocial development at age 3.

The findings are being published in the New England Journal of Medicine.

Dr. Heidi Feldman, one of the co-authors, said she expects the study may cause doctors and parents to think twice about the procedure. Though implanting the tubes is simple, placing small children under general anesthesia always carries risks and some children may suffer complications, such as hearing loss or discharges of pus. "I think it will reduce the number of by a half or two-thirds," she said of the study results.

But Dr. Christopher Post, a pediatric ear, nose and throat specialist at Allegheny General Hospital, cautioned that the study was narrowly focused and didn't address other reasons for the tubes, which he argues are more common: relieving the persistent ache associated with otitis media and helping eliminate the infection.
"I don't believe in tubes 'early and often,' " Post said. "Tubes are overdone." But many parents express relief after tubes are inserted and their children start sleeping through the night, he added.

In an editorial accompanying the Paradise article, Dr. James Perrin, director of general pediatrics at Massachusetts General Hospital, said health care providers should exercise caution when referring young children for ear tubes. Now that the procedure seems to have no effect on child development, doctors must consider whether reducing short-term hearing loss and decreasing the persistence of effusion are enough to justify its real, though apparently small, risks.

The study was massive in size, enrolling more than 6,000 infants in the early 1990s who were examined monthly until they were age 3. This enabled the researchers to identify children with otitis media who didn't have symptoms and also to know precisely how long fluid had been in the ear, Feldman explained.

During the study, 429 of these children developed substantial otitis media that persisted in both ears for more than three months. Half of these children were then immediately referred to surgeons for tube implants. Decisions were delayed for up to nine months for the other half; in most cases, the otitis media cleared up on its own, so only about a third of this group ended up with ear tubes.

Persistent fluid in the middle ear reduces the ability to hear. In a small child just learning language skills, it was feared that this temporary disability could cause delays in development that could last long after the ear inflammation had cleared up.

But tests at age 3 found no difference between the children who had tubes implanted immediately and the children who either did not receive tubes or had them implanted up to nine months later.

Further testing was performed at age 4; that data is now being analyzed, Feldman said. By the end of the year, testing will be complete on all of the children at age 6.

The study was funded in part by two pharmaceutical manufacturers, SmithKline Beecham and Pfizer. In years past, this might have constituted a conflict of interest, Feldman acknowledged, because the alternative to ear tubes was often continued use of antibiotics. But this is no longer the case, she maintained. In most cases, antibiotics are no longer recommended for children with fluid buildup in the ear who are otherwise healthy.

These include the obvious culprits such as alcohol and cigarette use, but serious new concerns are being raised by government and university research showing many common household chemicals are also being found to damage brain development during pregnancy.

These include cleaning chemicals, home pesticide use, cosmetic chemicals (such as nail polish and perfume), prescription medications, artificial food additives, chemicals in plastics, synthetic perfume and cologne ingredients, job chemicals, and the pesticide chlordane (found as a contaminant in the air of most U.S. homes built before 1988) .

In a summary report entitled the Principles of Developmental Neurotoxicity, from the National Center for Toxicological Research (7), it was stated:

"According to the Congressional Office of Technology Assessment’s recent report on neurotoxicity, among the known or suspected causes of brain-related disorders are exposure to chemicals including pesticides, therapeutic drugs, food additives, foods, cosmetic ingredients and naturally occurring substances"

If we are to agree with this research that repeated exposure to certain consumer chemicals can weaken or damage brain growth and result in increases in mental retardation, learning disabilities or behavior disorders, then it is quite plausible to expect a corresponding subtle decrease in mental function of our above average students, but detecting such effects will be extremely difficult.

Also, it is important to realize that a decrease in mental capacity is not strictly limited to academic function. The human brain is also responsible for all other mental functions including talent, personality, sense of humor, articulation skills and even conscience oriented behavior.

Therefore, it is quite realistic to suspect the potential for these areas of the human brain to be compromised by the same compounds being found to cause learning disabilities and attention deficit disorder.

Many researchers now agree, as will be addressed in this paper, that subtle brain disorders can be the cause of learning disabilities, hyperactivity, attention deficits and even propensity toward behavior problems such as aggression and behavior "void of conscience." In fact, it has been only recently that abnormalities in brain structure have been found in people with learning disabilities and attention deficit disorders.

Brain Damage Found in Students with Learning Disabilities and Attention Deficit Disorder.

Examples of visually detected brain damage in learning disability and attention deficit individuals are discussed in three different research projects below. One incident reported by Dr. Albert Galaburda at Harvard Medical School, investigated the unfortunate accidental death of an individual with known serious reading learning disabilities in school. At age 18 he had a reading level of fourth grade despite a 105 intelligence score on the Stanford- Binet test. Because of this discrepancy in intelligence and reading level, he was given the diagnosis of Developmental Dyslexia. He also had moderate math difficulties and mild difficulties with right-left orientation and finger recognition.

At age 20, six days after beginning his first paying job, the patient died suddenly as the result of an accidental fall from a great height. The cause of death was multiple internal injuries producing massive bleeding. An autopsy of the brain showed no evidence of trauma or other gross abnormalities according to the researchers. After receiving permission from the man’s parents, the physicians conducted a thorough examination of the man’s brain structure. The researchers stated the area of the learning disability brain shows abnormalities also to a location in the brain called the "Wernicke’s Speech Area," and appears to play a particularly important role in language function.

The researchers concluded by saying,
"The findings reported here lend support to the notion that language-relevant areas in the brains of patients with developmental dyslexia (a type of learning disability) may be small in the two cerebral hemispheres, a possibility which is also supported by findings of curtailed linguistic processing by both hemispheres in dyslexic patients."

Learning Disability & Attention Deficit Children Have Lower Blood Flow in Some Brain Areas

Department of Neurology, Kennedy Institute in Denmark

A method for determining abnormalities in the brains of living learning disability (LD) and attention deficit disorder (ADD) children was used in a study of 13 LD and ADD children at the Department of Neurology, Kennedy Institute in Denmark.

The study was conducted using a method called emission computed tomography which takes a picture of a "slice" of the brain after the child inhales a very small amount of a radioactive substance called xenon 133. The picture then allows the scientists to visually see how much blood is being used by different parts of the brain (a greater illumination in the picture represents increased blood flow). This also represents the level of metabolic activity in the brain areas. After comparing the photographs taken of all children the investigators stated,

"The cerebral blood flow distribution was abnormal in both hemispheres (both sides of the brains) in all patients, as compared with the mean cerebral blood flow distribution of nine normal children.... All 11 patients with attention deficit disorder (ADD) have hypoperfusion (low blood flow) in the mesial frontal lobes, in particular in the white matter.... Methylphenidate hydrochloride (Ritalin) increased perfusion (blood flow) in the central region, including the mesencephalon and the basal ganglia, and decreased perfusion of motor and primary sensory cortical areas.... Hypoperfusion and low metabolic activity may be due to subtle morphologic abnormalities not detectable with computed tomography but with important pathogenetic implications."

To bring this into perspective and without the multi-syllable medical terms, the investigators found lower levels of blood in Attention Deficit Disorder children in the area of the brain that is just behind the central forehead going in about an inch or two. When ritalin was given and measurements taken again, normal blood flow was created, thereby providing a biological explanation of why children improve after taking Ritalin.

Glucose Metabolism Defective in Attention Deficit Hyperactive Disorder Syndrome

In a study of hyperactive students conducted at the National Institute of Mental Health, reported in the November 15, 1990 New England Journal of Medicine, researchers found the brain cells of these individuals were using lower levels of glucose than other non-hyperactive people (glucose is the primary fuel used by the brain cells which enables them to function).

In a study of hyperactive students conducted at the National Institute of Mental Health, reported in the November 15, 1990 New England Journal of Medicine, researchers found the brain cells of these individuals were using lower levels of glucose than other non-hyperactive people (glucose is the primary fuel used by the brain cells which enables them to function).

In conclusion, the investigators stated:

"Glucose metabolism, both global and regional, was reduced in adults who had been hyperactive since childhood. The largest reductions were in the pre-motor cortex and the superior prefrontal cortex - areas earlier shown to be involved in the control of attention and motor activity."

Since there is common agreement among researchers and medical professionals that learning disabilities and attention deficits can, in fact, result from subtle brain damage caused by a variety of common environmental chemical exposures in today's "modern" society, it is imperative to organize this information into an easy to read format. This will give couples who desire to have children a far better chance of having a child that is neurologically healthy without the complications accompanied by attention deficit disorder or learning disabilities. This has been the goal of this research project.

An Interesting Observation from an Older Medical Journal

In the 1975 Canadian Psychiatric Association Journal, Dr. R. Denson discusses the increase society has observed in children with hyperactive disorders.
"The hyperkinetic syndrome is often encountered at the present time, although the textbooks of thirty years ago make scant reference to it. Henderson and Gillespie characterized hyperkinetic disease as one of the "very rare" psychoses of childhood, and Kanner, who devoted only five sentences to "the restless, fidgety, hyperkinetic child", omitted hyperactivity altogether when discussing the causes of scholastic problems.

Recent estimates imply that persistent, disruptive hyperactivity occurs in from five to ten percent of North American elementary school children and Wender who depicts hyperactivity as "the single most common behavioral disorder seen by child psychiatrists", has calculated that there are approximately five million hyperactive children in the United States, where more than 150,000 youngsters are receiving treatment with stimulant drugs for hyperkinesis and similar disorders."

For more information on the chemicals and job exposures being found to cause Attention Deficit Disorder, Attention Deficit Hyperactive Disorder, and Learning Disabilities, please visit www.chem-tox.com/pregnancy/learning_disabilities.htm

Food Allergies
Janet Zand L.Ac., O.M.D.

(Excerpted from Smart Medicine for a Healthier Child)


An allergy is a hypersensitive reaction to a normally harmless substance. About one in every six children in the United States is allergic to one or more substances. There are a variety of substances, termed allergens, that may trouble your child. Common allergens include pollen, animal dander, house dust, feathers, mites, chemicals, and a variety of foods. This section is devoted to food-related allergies.

Allergic reactions can occur immediately, or they can be delayed and take days to surface. A delayed allergic reaction can make it more difficult to pinpoint the allergen.

Common symptoms of an allergic reaction are respiratory congestion, eye inflammation, swelling, itching, hives, and stomachache and vomiting. Food allergies can contribute to chronic health problems, such as acne, asthma, bedwetting, diarrhea, ear infections, eczema, fatigue, hay fever, headache, irritability, chronic runny nose, and even difficulty maintaining concentration (attention deficit disorder, or hyperactivity). Food allergies can also cause intestinal irritation and swelling that interferes with the absorption of vitamins and minerals. Even if you are providing your child with a wholesome, nutritious diet, if she is consuming foods to which she is allergic, she may not be able to absorb food properly, and therefore may not be deriving the full benefits of all the foods she is eating.

The most common foods that cause allergic reactions in children are wheat, milk and other dairy products, eggs, fish and seafood, chocolate, citrus fruits, soy products, corn, nuts, and berries. Many children also are allergic to sulfites, which are found in some frozen foods and dried fruits, as well as in medications. Some people seem to be genetically predisposed to food allergies. If family members, especially parents, have food allergies, there is a greater chance a child will have the same difficulties.

Sometimes, if all the irritating foods are eliminated from a child's diet for several months, her body will have a chance to rest and heal, after which it will be able to handle small amounts of these foods without reacting. Sometimes, too, there is an underlying issue such as a parasitic or yeast infection in the intestine that is contributing to the allergic response. If these underlying problems are cleared up, the child's body may be less reactive to certain substances.

It has been observed that some children actively dislike the foods that produce an allergic reaction. They seem to know instinctively that certain foods will cause a problem. If your child continually refuses particular foods, it may be wise not to force the issue.

Paradoxically, however, some children seem to be particularly drawn to the very foods that cause a problem. For example, many children are allergic to peanut butter, a staple in many homes. Children who continually ask for peanut butter, or those who enthusiastically eat lots of wheat bread, wheat crackers, and wheat cereals, or who crave milk, ice cream, and other dairy products, may actually be exhibiting an allergy to those foods.

EMERGENCY TREATMENT FOR FOOD ALLERGIES
Occasionally, an allergic reaction is so severe it can be life threatening. If your child exhibits rapidly spreading hives or has difficulty breathing, seek medical attention immediately.

If there is any sign that your child is having difficulty breathing due to a severe allergic reaction, especially if she has a history of severe reactions, take her immediately to the emergency room of the nearest hospital. If you cannot transport your child yourself, call for emergency help and stress the urgency of the situation. Every second counts.

If an emergency adrenaline kit, such as the Ana~it or EpiPen, is available, administer it immediately, followed by 50 milligrams of an antihistamine such as Benadryl. Do not give your child anything to eat or drink if she is having difficulty breathing. Even if your child responds quickly to the administration of the emergency adrenaline kit, she should still be taken to the emergency room for professional evaluation and treatment.

Conventional Treatment
The most important part of treating food allergies, obviously, is to identify- and then avoid-the foods that are causing your child's reaction. There are two techniques, the elimination diet and the rotation diet, that enable you to do this. Once you have identified the foods or classes of foods that cause symptoms in your child, remember to read the labels on all the processed food products you buy. Many food products will contain one or more of the substances you have identified as the source of your child's allergy.

In cases of severe multiple food allergies, oral cromolyn sodium (Gastrocrom) may be prescribed as a preventive measure. This is the same drug that is used in inhaled form to prevent asthma attacks.

If your child suffers from recurrent allergic reactions, an antihistamine may be recommended.

Dietary Guidelines
Use an elimination diet to determine which foods are causing your child's symptoms. Some of the foods that most commonly cause a reaction are dairy products, wheat, citrus fruits, nuts (including peanut butter), corn, soy products, cane sugar, and eggs. You may wish to try eliminating these first.

Always read product labels and be aware of the ingredients in manufactured food products, especially additives such as artificial flavorings and colorings. Processed foods often contain a surprising array of ingredients and additives. It's better to base your child's diet on whole foods that you prepare yourself.

Nutritional Supplements
For age-appropriate dosages of nutritional supplements, see Dosage Guidelines for Herbs and Nutritional Supplements.

Calcium and magnesium help to reduce sensitivity and nervousness associated with allergies. Give your child a combination liquid containing 250 milligrams of calcium and 125 milligrams of magnesium, twice a day, for two to three months.
Give your child 50 to 100 milligrams of pantothenic acid, twice daily, at least one hour away from food, for one month to support adrenal function.

The B vitamins help support adrenal function. Give your child a vitamin-B complex supplement, twice a day, for two to three months.

Vitamin C helps to stimulate immune function. Give your child one dose of vitamin C, in mineral ascorbate form with bioflavonoids, twice a day, for two to three months.

General Recommendations
Use an elimination or rotation diet to identify the food or foods that are causing your child's allergic response.

Because allergic reactions can take a wide variety of forms, from headaches to bedwetting, you may want to consult other entries in this book that correspond to your child's symptoms.

Prevention
There is no way to prevent your child from developing a food allergy. It goes without saying, however, that you should make sure she is not exposed to any known allergens.

Cycled Light Promotes Growth in Pre-Term Infants, Duke University Study Finds

DURHAM, N.C., Feb. 21 (AScribe Newswire) -- A Duke University Medical Center study has shown that exposing babies born before 31 weeks of gestation to cycled light helps them grow faster, and the study identifies no short-term advantages to keeping infants in total near darkness -- the standard practice with many infants.

According to the nurse researchers, by growing faster such pre-term infants can leave the hospital sooner and may have improved developmental outcomes. The study is published in the February 2002 issue of the Journal of Pediatrics.

Approximately 10 percent of all pregnancies in the United States result in pre-term births. A baby is considered pre-term if born before 37 weeks gestation. A full-term pregnancy is 37 to 40 weeks gestation.

Pre-term deliveries are costly both financially and emotionally for families, and the infants are at risk for multiple health and developmental problems. By creating an environment that may encourage growth, the Duke research suggests, these pre-term complications may be reduced.

"Additional research will be needed to show the long-term impact of a cycled light environment in these babies, but this research clearly shows that cycled light improves growth rates in pre-term babies, and that's a step in the right direction," said Debra Brandon, Ph.D., R.N., principal investigator and associate professor in the Duke School of Nursing.

Currently, many neonatal intensive care units keep babies in near darkness to simulate the mother's womb. Constant bright light has been shown to be too stressful on pre-term infants, causing irregular heart rates and decreased sleep. However, until the Duke study, no research has examined the benefits of cycled light versus near darkness.

"Cycled light establishes a day/night rhythm, mimicking the circadian rhythm cues that are established for full-term babies in the womb," said Brandon. "We know adults rely on circadian rhythms for health, growth and development, and pre-term babies grow within a rich circadian environment provided by the mother. Therefore it is likely that a circadian environment is important for pre-term infants. Light is one method that we can use to promote circadian rhythms for these infants and encourage growth and healthy sleep patterns."

Researchers from the schools of nursing at both Duke and the University of North Carolina at Chapel Hill (UNC-CH) examined the effects of cycled light on 62 infants born before 31 weeks gestation at Duke University Hospital and Durham Regional Hospital. Infants with neurologic or visual problems were excluded from the study.

The babies were assigned randomly to three groups: cycled light from birth, cycled light once they reached 32 weeks postconceptual age (equivalent to gestational age if the baby had not been born pre-term) and cycled light at 36 weeks postconceptual age. Infants in all three groups were similar with respect to degree of prematurity and birth weight.

The babies were weighed daily. Infants who received cycled light from birth and cycled light at 32 weeks postconceptual age grew more rapidly than the babies who received cycled light just before discharge.

"Now that we know that cycled light does encourage growth in the short term, we need to also follow these babies for long-term impact," said Brandon. "In two to five years, will we see that these babies have continued to grow well? Will they have developed sleep patterns earlier and have better language and cognitive development? We need to know the answers to these questions."

The National Institute of Nursing Research, a division of the National Institutes of Health, funded the research.
Co-authors on the paper include Diane Holditch, Ph.D., R.N., and Michael Belyea, Ph.D., of UNC-CH School of Nursing.

The study found that the lowest and most conservative estimate of AD/HD occurrence among the study subjects was 7.5 percent by age 19, based on research criteria for AD/HD. These criteria required both a clinical diagnosis of AD/HD and supporting documentation in the medical and school records.

"The 7.5 percent incidence of AD/HD from the current study includes subjects who met the most stringent research criteria and are likely to represent cases that most clinicians would regard as true cases of AD/HD," says William Barbaresi, M.D., a Mayo Clinic developmental and behavioral pediatric specialist and lead author of the study. "This study represents what we believe to be the largest population-based study of the occurrence (incidence) of AD/HD to date."

The AD/HD cases in the Mayo study were identified on the basis of rigorous research criteria, including a clinical diagnosis and extensive supporting documentation. Researchers also obtained comprehensive information about study subjects from both medical and school records.

A number of previous studies of the incidence of AD/HD relied on limited sources of information to establish the diagnosis. For example, some included only a single teacher questionnaire or lay-administered diagnostic interview.

"We took a hard look at this condition from a number of angles to help pinpoint the occurrence rates," says Dr. Barbaresi. "The results from this study provide much needed baseline information for comparison with populations in other communities. We believe this information will help us to determine how many children in the United States have AD/HD, and therefore, how many should be expected to receive treatment for this condition."

The study subjects included a total of 8,548 children born between Jan. 1, 1976, and Dec. 31, 1982, to mothers residing in the five Olmsted County, Minn., townships comprising Minnesota Independent School District #535.

AD/HD is a chronic disorder that begins in childhood and sometimes lasts into adult life. In general, children and adults with AD/HD have a difficult time paying attention and concentrating (inattention), sitting still (hyperactivity) and controlling impulsive behavior (impulsivity). These problems can affect nearly every aspect of life. Children and adults with AD/HD often struggle with low self-esteem, troubled personal relationships and poor performance in school or at work.

The study was supported by research grants from National Institutes of Health and Mayo Foundation.

What is it?
An auditory processing disorder interferes with an individual's ability to analyze or make sense of information taken in through the ears. This is different from problems involving hearing per se, such as deafness or being hard of hearing. Difficulties with auditory processing do not affect what is heard by the ear, but do affect how this information is interpreted, or processed by the brain.

An auditory processing deficit can interfere directly with speech and language, but can affect all areas of learning, especially reading and spelling. When instruction in school relies primarily on spoken language, the individual with an auditory processing disorder may have serious difficulty understanding the lesson or the directions.

Common areas of difficulty and some educational implications:

Phonological awareness
Phonological awareness is the understanding that language is made up of individual sounds (phonemes) which are put together to form the words we write and speak. This is a fundamental precursor to reading. Children who have difficulty with phonological awareness will often be unable to recognize or isolate the individual sounds in a word, recognize similarities between words (as in rhyming words), or be able to identify the number of sounds in a word. These deficits can affect all areas of language including reading, writing, and understanding of spoken language.

Though phonological awareness develops naturally in most children, the necessary knowledge and skills can be taught through direct instruction for those who have difficulty in this area.

Auditory discrimination
Auditory discrimination is the ability to recognize differences in phonemes (sounds). This includes the ability to identify words and sounds that are similar and those which are different.

Auditory memory
Auditory memory is the ability to store and recall information which was given verbally. An individual with difficulties in this area may not be able to follow instructions given verbally or may have trouble recalling information from a story read aloud.

Auditory sequencing
Auditory sequencing is the ability to remember or reconstruct the order of items in a list or the order of sounds in a word or syllable. One example is saying or writing "ephelant" for"elephant".

Auditory blending
Auditory blending is the process of putting together phonemes to form words. For example, the individual phonemes "c", "a", and "t" are blended to from the word, "cat".

Neuropsychological and neurophysiological indices of auditory processing impairment in children with multiple complex development disorder.
Journal of the American Academy of Child and Adolescent Psychiatry
Author/s: Alan J. Lincoln

Several investigations have revealed a characteristic pattern of behavioral and emotional dysfunction in children that has been referred to as borderline personality disorder or borderline disorder (BD) (Bemporad et al., 1982; Guzder et al., 1996; Kernberg, 1982; Pine, 1986) and more recently characterized as "multiple complex developmental disorder" (MCDD) (Cohen et al., 1987; Towbin et al., 1993; Van der Gaag et al., 1995). Although the labels of BD or MCDD are controversial (Towbin et al., 1993), these children are likely to represent a significant percentage of the childhood psychiatric inpatient population. In an adult outcome study, such individuals continued to manifest significant psychopathology in later life (Lofgren et al., 1991).

Cohen et al. (1987) delineated three primary core symptoms found in children with MCDD. These include (1) the impaired regulation of affect states and anxiety, (2) consistent impairments in social behavior, and (3) impaired cognitive processing (thought disorder). BD/MCDD children appear to manifest extreme fluctuations in cognitive, attention, and emotional functioning (Bemporad et al., 1982; Towbin et al., 1993). Comorbidity between BD/MCDD and other disorders of childhood, such as attention-deficit hyperactivity disorder (ADHD), is evident in many cases (Bemporad et al., 1982; Boksenbaum, 1993; Guzder et al., 1996; Towbin et al., 1993).

Impairments of attention regulation in children with ADHD are well documented. (Agrawal and Kaushal, 1987; Hamlett et al., 1987; Pearson et al., 1991; Swanson et al., 1991). Attention impairments have also been associated with pathophysiology in individuals with ADHD. Abnormalities of event-related potentials (ERPs) associated with attention, the P300 in particular, have been described in persons with ADHD (Bloom, Lincoln, Courchesne, and Johnson, unpublished; Loiselle et al., 1980; Robaey et al., 1992; Satterfield et al., 1990).

ERPs are derived by averaging EEG to time-locked stimulus events. In such an averaging process, EEG that is not correlated with the onset of an experimentally controlled stimulus is averaged out, while EEG correlated with the experimentally controlled stimulus is retained in the average. This process results in recognizable ERPs that are defined by their topography, voltage (in microvolts), and latency (in milliseconds from either the onset of the time-locked stimulus or time-locked behavior response).

An ERP component, P300 (also referred to as P3 and includes both P3a and P3b), has been studied extensively in nonpatient populations (Hillyard and Picton, 1987, review; Johnson, 1986, 1993, review; Lincoln et al., 1993; Pritchard, 1981, review).

The P300 is typically elicited by the use of an "oddball" paradigm in which the subject is directed to respond behaviorally to an infrequent target stimulus that occurs within a series of more frequently occurring nontarget stimuli.

The amplitude of P300 has been suggested to represent a variety of factors involved in attention processing, including the updating of the current cognitive schema regarding the stimulus (Donchin, 1981; Donchin and Coles, 1988). The amplitude of P300 is thought to reflect the culmination of several factors that include stimulus modality, stimulus probability, and stimulus meaning (Johnson, 1986, 1993).

In both the auditory and visual modalities the amplitude of P3a and P3b are sensitive to changes in the probability of target stimuli; the amplitude of each component increases as the target stimulus probability decreases (Johnson, 1986, 1993). The P300 also decreases in latency (the time from the onset of the stimulus to when its peak amplitude is reached) from childhood through early adolescence (Courchesne and Yeung-Courchesne, 1978).

Thus, it takes children more time than adolescents or adults to cognitively register that a stimulus event has occurred. Generally, the time required for a behavioral response (reaction time) to the target stimulus is longer than the cognitive response as indexed by the P300. In children the P300 may reflect overlapping components: the P3a, which has a more frontal-central distribution and is of earlier latency, and the P3b, which has a more posterior distribution and is of later latency.

A delighted mum has told how she finally unlocked her sons' silent world by changing their diet - and scrapping junk food.

Sandy Armstrong, 42, was horrified when Tom and Andrew stopped speaking at 18-months-old and started suffering epileptic fits. They were diagnosed with the rare Landau Kleffner Syndrome, a neurological disorder which results in the loss of language development.

Doctors prescribed high-dose steroids and anti-epilepsy drugs. But after swotting up on the illness desperate Sandy tried them on a strict gluten and dairy free diet and banned junk food.

Incredibly, 12 months later Tom and Andrew were weaned off the drugs, their language returned and they haven't had a fit since. Relieved Sandy, of Bristol, is now living a happy family life with husband Mike, 47, Andrew, now nine, and Tom, eight.

She said: ''It was horrendous - sometimes the fitting was so bad they couldn't sleep. There was no way they could live a normal life. ''In desperation I tried them on a strict diet and Andy's language is now back to normal and Tom is much, much better.

''It is incredible. I hate to think what situation we would be in without the diet.''

A spokeswoman for Clover House, a nutritional charity in Bristol, said: ''Food can often have an incredible effect on people's lives.
''Evidence suggests some people cannot digest wheat and diary products completely and the proteins leak into the bloodstream and into the brain.''

If some of the stuff in your kitchen is bad for you, it stands to reason that some of the rest of it ought to be good for you. We already know about bran, carrots, spinach, kale, leeks and seaweed, but now, scientists may have discovered an even more palatable way for us to stay healthy.

This new health drink is a special kind of tea. It's been shown to significantly reduce the effects of carcinogens in laboratory mice. It slowed the development of skin cancer in mice exposed to UV radiation. It helped slow or prevent the formation of stomach and lung cancer tumors (in mice). And, in one study, using one of the most potent carcinogens in cigarette smoke, mice given this type of tea developed 45% fewer lung cancer tumors.

In Japan, where they consume a lot of this beverage, the death rate from lung cancer is much lower than here in the United States, even though the average cigarette consumption among men in Japan is much higher.

What is this special tea with all the potential health benefits? It's not chamomile, or rosehips, or bran, carrots, spinach, kale, leeks or seaweed, for that matter. It's tea. Just ordinary tea. Green tea to be exact, from your typical tea plant, Camellia Sinensis. Scientists currently believe that the active ingredient that may be responsible for the anti carcinogenic effects are the group of polyphenols called catechins. Dry black tea, like your ordinary grocery tea, contains 3%-10% catechins. Oolong tea contains a little bit more (8-20%). Green tea, however, contains a lot more. A full 30-42% of the dry weight of green tea consists of catechins.

All of these different styles of tea are made from the same plant--the difference is in the processing. Black tea is made by rolling the leaves, then exposing them to air. This causes most of the polyphenols in the leaves to oxidize. Oolong tea is produced via a process of rolling and drying that causes only about half of the polyphenols to be lost. Green tea, however, is heated with dry air or steam, and this destroys the enzyme in the leaves that allows the polyphenols to oxidize. They remain in the leaves to benefit mankind and laboratory mice.

Further research is needed to pin down the specific health benefits of green tea to humans, because there's no way to know for certain, via statistical research, where the health benefits are coming from. in order words, if you are the type of person who prefers green tea, you may also be the type of person who does many other health things.

In the meantime, a couple of things seem certain. First, it if turns out that the risk of cancer can be reduced by something as simple as drinking a cup of tea, we can expect to be hearing a lot more about it. Finally, to paraphrase one researcher, a cup or two a day can't hurt!

Ms. Lewis' book helps provides answers to many questions parents may have about the diet. It is a wonderful resource of information for anyone who is considering the GFCF Diet or has already begun. The book also contains over 150 wonderful recipes that are gluten and casein free.