April 2004

Models of Attention John G Taylor, PhD Models of attention have a venerable history going back to Aristotle, who considered attention as a narrowing of the senses. More recently, numerous experiments have been performed to discover brain regions involved in various aspects of attention. Using global functional brain imaging techniques (PET and fMRI) various experiments have shown that moving the focus of attention is achieved by a different brain network from that involved in processing the input being attended to [1, 2]. The regions exercising control of attention movement are in parietal and prefrontal sites, while attended sites are in primary and secondary cortices in the various senses (and also in motor cortex for response). These locations have been supported by study of deficits in the speed of attention movement, as shown from studies by Posner and colleagues [3]. Attention modulates activity in the input sites, as shown both globally from fMRI data in attention paradigms [4] and by analysis of single cells in monkey early visual cortex [5]. Attention achieves its effects on earlier cortical sites by feedback, which changes the classical receptive fields of cells in anaesthetised monkeys as compared to awake animals [6]. Detailed timing analyses in humans, using EEG and fMRI methods, support the existence of attention-controlled feedback [7], as well as the general model of control arising from superior parietal sites in the fast dorsal steam to gate slower object representations in the ventral stream [8] Attention control has been found to arise by two mechanisms, one by bottom-up signals from the occurrence of unexpected and strong inputs (such as a brief flash of light), the other by top-down control from some required goal (such as by the face of a friend being searched for in a crowd). It had been thought that bottom-up signals normally achieved attention capture; it is now appreciated that top-down control is usually in charge. Involuntary attention capture by distracting inputs occurs only if they have a property that a person is using to find a target [9]. Thus there is a single control network deciding between the importance of desired (top-down) and unexpected (bottom-up) sites for attention. The lack of attention capture has been carefully investigated as has the phenomenon of inattentional blindness, in which apparently important and unexpected events just do not draw our attention to them [10, 11]. The two sorts of attention, termed exogenous for bottom-up and endogenous for top-down, have been found to possess quite different times for onset and decay: exogenous attention is rapid, and reaches its maximum effect about 100-200 msecs after cue onset in humans, and then falling away as rapidly. On the other hand endogenous attention is slower, rising gradually to a maximum only at about 300-400 msecs after cueing occurs. Attention can be divided between two modalities, such as vision and audition, but the degree of coupling of the control over attention in different modalities is still controversial [12]   Recent Models of Attention Theoretical models of attention have been produced which try to keep up with the rapid pace of experimental advance described above. These models are of two sorts. One is psychological/ functional, and leads to insights into information flow but not to quantitative comparisons with data. The other uses neural networks, and provides detailed simulations of psychological paradigms by interacting neurons in modules that may or may not be part of the psychological models. These latter models can therefore be more stringently tested. There are now numerous neural network models of attention; only outlines of a selection of them can be considered. The first psychological model [13] dissociates the overall control of attention into: alert ® interrupt ® localize ® disengage ® move ® engage ® inhibit. Evidence has been brought forward to support such a dissociation, with various modules, including the pulvinar nucleus in thalamus, as running the separate stages. A second approach [14] is based on selection of an area in visual space, using both inhibitory and excitatory mechanisms in a separate module to identify objects, and the movement of attention is then achieved by sliding down the gradient of an excitatory hill in another competitive network. A third model also uses biased competition to move attention to objects [15]. These and related models use a form of competition in a higher-level module to guide movement of attention on a lower order one. Neural network simulations of attention tasks implement this general idea. Simulation of visual search times for targets in the presence of distracters has been performed using an input module (representing early visual cortex), a higher order module where a competition determines where attention shall be focused (as in parietal lobe), and an object-coding module to represent objects learnt in the past (as in temporal cortex). A linear increase in search time with number of distracters has been observed in such simulations [16, 17]. Biasing the competition for attention by a frontal template has also been studied in a model with explicit frontal sites [18]. Finally both a salience-based approach and a synchronized oscillator method have been developed which cause object segmentation in cluttered scenes followed by attention orienting [19, 20]. An explicit engineering control framework has been introduced which fuses these approaches [21]. It uses a plant site (identified as early cortex and temporal lobe), an inverse control module (identified as in parietal lobe), a rules module (in prefrontal cortex) and an observer or forward model (with components in both parietal and prefrontal lobes).This model leads to close agreement of the dependence of response speed-up achieved by attention to a target as the cue-to-target time interval varies from 0 to 1.5 seconds. The calculated rise and fall of the exogenous attention shift benefit and the slower but steady rise of the endogenous shift benefit possess the features observed in humans mentioned earlier [22].Detailed contributions of some of the control components are still being assessed. References [1]. Hopfinger JB et al (2000) The neural mechanisms of top-down attentional control. Nat Neurosci 3:284-291. [2]. Kastner S & Ungerleider LG (2000) Mechanisms of Visual Attention in the Human Cortex. Ann Rev Neurosci 23:315-341. [3]. Posner M & Petersen SE (1990) The Attention System of the Human Brain. Ann Rev Neurosci 13:25-42. [4]. Friston KJ et al (1995) Characterizing Modulatory Interactions Between Areas V1 and V2 in Human Cortex: A New Treatment of Functional MRI Data. Hum Brain Map 2:211-234. [5]. Reynolds JH et al (1999) Competitive Mechanisms Subserve Attention in Macaque Areas V2 and V4. J Neursoci 19:1736-1753. [6]. Lamme VF & Roelfsema (2000) The distinct modes of vision offered by feed-forward and recurrent processing. Trends Neurosci 23:571-579. [7] Martinetz A et al (2001) Putting spatial attention on the map. Vis Res 41:1437-1457. [8] Vidyasagar TR (1999) A neuronal model of attentional spotlight: parietal guiding the temporal. Brain Res Revs 30:66-76. [9]. Pashler H (2001) Attention and Performance. Ann Rev Psych 52:629-51.  [10]. Mack A & Rock I (1998) Inattentional Blindness: Perception without Attention. Ch 3, pp 55-76 in visual attention, ed RD Wright. Cambridge MA: MIT Press..  [11]. Simms DJ (2000) Attentional capture and inattentional blindness. Trends Cognit Sci 4:147-155. [12]. Spence C et al (2000) Cross-modal selective attention: On the difficulty of ignoring sounds at the locus of visual attention. Proc Psychophys. 62:410-424. [13] Posner MI et al (1987) Isolating attentional systems: a cognitive-anatomical analysis. Psychobiology 15:107-121. [14] LaBerge D & Brown V (1989) Theory of Attentional Operations in Shape Identification. Psych Rev 96:101-124. [15] Desimone R & Duncan J (1995) Neural Mechanics of Selective Visual Attention. Ann Rev Neurosci 18:193-222.  [16] Mozer MC & Sitton M (1999) Computational modeling of spatial attention. Ch 9, pp 341-393 in Attention. ed H Pashler. New York: Taylor & Francis. [17] Deco G & Zihl J (1998) A Neuronal Model of Binding and Selective Attention for Visual Search. Pp 262-271 in Cognitive Neuroscience, Heinke D, Humphreys GW & Olson A (eds). London: Springer. [18] Jackson SR et al (1994) Networks of Anatomical Areas Controlling Visuospatial Attention. Neural Networks 7:925-944. [19] Lee DK, Itti L, Koch C, Braun J. (1999) Attention activates winner-take-all competition among visual filters. Nature Neurosci 2(4):375-81. [20] Fellenz W (1994) A sequential model for attentive object selection. In Proc 39th IWK Conf, Ilmenau. [21] Taylor JG (2001) Attention as a Neural Control System. pp 272-276 in Proc Int Joint Conf on Neural Networks (IJCNN’01), IEEE Cat #01CH37222C, ISBN# 0-07803-7046-5. [22] Taylor JG & Rogers M (2001) A control model of the movement of attention. Neural Networks 15: 309-326.   The Author John G Taylor Department of Mathematics, King’s College, Strand, London WC2R2LS, UK ------------------------------------------------------------------------ Published on 31.December.2002 Copyright 2002 Universidade Estadual de Campinas Brain & Mind Magazine An initiative: Center for Biomedical Informatics

ADD/ADHD

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Understanding And Dealing With Attention Deficit & Hyperactivity Disorders Revised: March 25, 2004 Medications used to treat ADHD do not correct known chemical abnormalities, they create new ones.   The stimulants used to treat ADHD are addictive and can cause serious brain abnormalities.   Attention Deficit Hyperactivity Disorder (ADHD) is by definition a disorder that first occurs in childhood and may persist into adulthood.  ADHD is a relatively common psychiatric condition and is responsive to treatment.  The essential features are a persistent pattern of inattention and/or hyperactivity with impulsivity.  Inattention is an impaired ability to maintain a focused awareness and to recognize details, objects, as well as elements in a task, communication or sequence of events.  Hyperactivity means "extra-active".  The inclusion of the term hyperactivity has fallen in and out of favor and was recently reintroduced as an addition to the term attention deficit.  It is unclear whether or not hyperactivity is actually part of the condition or a separate condition.   Impulsivity is a tendency or pressure to act without a level of restraint that would be normal for the person's level of development.  A person with ADHD has difficulty moderating and controlling their behavior.  They appear consistently driven, internally pressured and have difficulty remaining focused while participating in activities that many of us would find easy. The key to recognizing ADHD is an awareness of what constitutes age appropriate behavior in different environments. There is good reason to be concerned whether a child has ADHD.  The behaviors and symptoms can make normal adjustment difficult.  ADHD occurs in 3 to 5% of all school age children.  The disorder occurs 4 to 9 times more often in males than in females.  Data on the prevalence in adolescent and adult populations is very limited.  In most cases, symptoms diminish by adolescence and early adulthood.  ADHD-like behaviors tends to be more prevalent in children where there is a history of that behavior in family members.   This does not mean that ADHD is inherited. Attention Deficit Hyperactivity Disorder is one of the most misunderstood diagnostic categories in mental health.   What is most apparent about children with ADHD are the differences in their attention and activity level. These differences are dramatically noticeable when these children are required to maintain their attention during dull, boring and repetitive tasks.  There are a growing number of adults who believe they have ADHD.  The diagnosis of ADHD in an adult requires an evaluation of how that person functioned as a child.  Such retrospective diagnoses are in most cases extremely difficult, if not impossible.  If the person has any knowledge of the disorder or  investment in being diagnosed, it will be very difficult for the adult to give an accurate report.  Diagnosis of ADHD is not a simple matter although many parents, teachers and some mental health professionals are quick to make it.  For many parents, having a diagnosis of a problem behavior pattern and hearing the problem can be treated with medication is not only a relief but can help restore balance to an otherwise disruptive home environment.  Many scientists and mental health professionals argue that the symptoms used to diagnose ADHD are overly inclusive and end up diagnosing children with ADHD who are not disordered.   It is worth noting that the observed symptoms of ADHD in a particular child will vary considerably across settings and caregivers. Symptoms in large classrooms with boring topics that provide little interaction produce more ADHD symptoms that are smaller in classrooms with more frequent one-on-one interactions and more interesting activities. ADHD is a controversial diagnosis with little or no scientific or medical basis.  There is no solid evidence that ADHD is a genuine disorder or disease of any kind.  In fact, there are a growing number of scientists and mental health professionals who feel that ADHD is not really a disorder but rather part of the human condition.  Many professionals believe the diagnostic system used to classify the behavior of inattentive overly active children does more harm than good.  Many diagnostic labels have been created that describe children who have a low attention span, impulsive tendencies, and difficulty maintaining "normal" activity levels in response to a demanding situation.  The question is whether or not these behaviors are abnormal and represent a disorder.  Medication is by far the most common treatment for ADHD.  The number of children diagnosed and treated with medication for ADHD has increased 7 fold in the past 3 years. Several million children are being treated with Ritalin, stimulants and antidepressants on the grounds that they have attention deficit-hyperactivity disorder and suffer from inattention, hyperactivity, or impulsivity. Drugs used in the treatment of ADHD include: Ritalin (methylphenidate) Dexedrine and DextroStat (dextroamphetamine or d-amphetamine) Adderall (d-amphetamine and amphetamine mixture) Desoxyn and Gradumet (methamphetamine) Cylert (pemoline)Imipramine Interestingly, there is no proof of any physical abnormalities in the brains or bodies of children who are routinely labeled ADHD. They do not have known biochemical imbalances or "crossed wires."   Medications used to treat ADHD do not correct known chemical abnormalities, they create new ones.   The stimulants used to treat ADHD are addictive and can cause serious brain abnormalities.   There is a great deal of research to confirm that environmental problems can cause ADHD-like symptoms.  But regardless of the cause, the impact of inattention, hyperactivity and impulsivity can be detrimental to normal development.   Educational systems, employers and social expectations can be rather rigid.   Conflict and failures shape our sense of life, self-esteem, our ability to learn and our ability to get along with others.  Information And Steps You Can Take That May Help Consult with a qualified mental health professional who is competent and experienced at diagnosing and treating ADHD.  Get more than one professional opinion. Consult with a professional who supports the use of medication and a professional who is opposed to the use of medication unless absolutely necessary. In order to a make a diagnosis, it is important to: Explore all of the possibilities that could explain the child's behavior. Determine if there are any problems such as learning disabilities, conduct disorders, depression, anxiety or medical concerns. Fully evaluate the family structure, classroom situation, and any special conditions or problems. Evaluate the child's thinking and academic abilities. The Attention Deficit Dilemma Disorder, Deficiency, or Denature? Has the human brain suddenly become so dysfunctional that nearly 10% of the children in the West are suspected of having mental disorders that manifest as attention-deficits and hyperactivity? Or, could it be that our modern environment has something to do with it? Alternative approaches to ADD/ADHD really begin with an alternative view of this over-diagnosed and under-treated phenomenon. For example, ADD expert and author Thom Hartmann believes that some behavior diagnosed as ADD is not a disorder. Instead, it represents natural adaptive traits of personality and metabolism that in an evolutionary sense represent important survival skills. "This state of mind evolved naturally. It's not a malfunction — to the contrary, it's a coherent, functioning response to a different kind of world and society than that in which many of us live." Nothing is wrong with the so-called ADD child, he explains. They are simply "hunters in a farming society." We need to stop labeling these children as disordered. Instead, refer to them as "hunters" or "lookouts." A Different Perspective Writing in his landmark 1993 book, Attention Deficit Disorder: A Different Perception, Hartmann contends that behavior considered disorderly in the context of ADD has an equally valid and positive interpretation. For example: * "Distractible" translates into constantly monitoring the environment. * "Impatient" means results-oriented, acutely aware of whether the goal is getting closer, now. * "Impulsive" really means flexible, ready to quickly change strategy. * "Short attention span" suggests being able to throw oneself into the chase on a moment's notice. * One who "acts without considering the consequences" is willing to take risks and face danger. * "Daydreamers" are bored by mundane tasks; they like new ideas and enjoy the excitement of the hunt. Seeing ADD in this new light can remove the stigma of deficit and illness. Hartmann hopes this new perception will lead to positive ways of accommodating these hunters in contemporary society, allowing them "to again become the powers behind cultural, political, and scientific change which they have so often historically represented." After all, today Benjamin Franklin and Thomas Edison would probably be diagnosed with ADD. What's Stress Got to Do with It? Being a hunter in a farming society is obviously a stressful situation, as is much of modern life itself. As the hunter-sex, boys are diagnosed with ADHD seven-times more often than girls. Also, boys account for 70% of kids with learning disabilities, 80% of juvenile cases, and 83% of suicides among 15-19 year olds. The current scientific consensus on ADHD points to an imbalance in the brain chemical dopamine. Dopamine is related to the stress hormone adrenalin. Both are excitatory neurotransmitters known as catecholamines, which are involved with mediating the bodies' response to stress. One of the most vulnerable key neurotransmitters, dopamine levels are depleted by poor sleep or stress. Alcohol, caffeine, and sugar all seem to diminish dopamine activity in the brain. It's also easily oxidized, therefore adequate intakes of vitamins C and E are necessary to protect dopamine-using neurons from destruction by free radicals. A 1998 study at the University of Massachusetts Medical School measured levels of the stress hormone cortisol in subjects with ADHD. It concluded that "an impaired response to stress may be a marker for the more developmentally persistent form of the disorder." Stress also stimulates the breakdown of serotonin, a calming neurotransmitter that balances dopamine. What's more, serotonin plays a role in mediating allergic reactions. Since brain allergies are implicated in ADD, this reinforces the connection between ADD and stress. Drugs and Children In a November 1999 health watch segment, a major television network reported that ADHD may be caused by allergies to a wide range of possible substances — from chemical additives and colorings to foods such as dairy, chocolate, and wheat. Rather reluctantly, the medical correspondent suggested that perhaps parents could find out which foods were the problem. She made it sound like a lot of trouble, however, to monitor what your child eats in order to identify the allergens. The underlying message was that it is simpler to just give them a drug. This came as no surprise — a pharmaceutical company sponsored that health watch segment. Even on their web page, drug ads predominated, although the ADHD report was absent. Stimulants have been used to treat ADHD since the 1930s. Most recently, these medications include methylphenidate (Ritalin) and dextroamphetamine (Denedrine). Another drug, Cylert (pemoline), was withdrawn in Canada in September 1999 due to the possibility of serious liver complications. These medications increase nervous system alertness by prompting an increased production of the neurotransmitters dopamine and norepinephrine, enhancing attention while reducing excess restlessness. Prescriptions of Ritalin have multiplied, especially for very young children. In 1995 it was estimated that more than 1.5 million American children aged 5 to 18 were taking Ritalin. One recent study found that 18-20% of the fifth-grade white boys in two cities had been diagnosed with ADHD and were being treated with stimulant drugs. A strongly-worded report titled "Diet, ADHD, and Behavior" was released in November 1999 by the nonprofit Center for Science in the Public Interest (CSPI). Among its findings: "The U.S. Drug Enforcement Administration (DEA) of the U.S. Department of Justice, which treats methylphenidate as a controlled substance, reports that manufacturers' sales increased nearly five-fold between 1990 and 1998 and that the U.S. now consumes 90 percent of the methylphenidate produced throughout the world. While prescriptions for methylphenidate began leveling off between 1995 and 1997, prescriptions for amphetamines, which are also used to treat ADHD, tripled, so overall use of stimulant drugs has continued to rise. One reason for the increase is that more elementary-school children are remaining on those drugs into their teens." Evidence suggests that the problem is growing. At a November 1999 medical conference devoted to the disorder, it was estimated that attention deficit hyperactivity disorder affects from 10-15% (1.8 to 2.7 million) of all U.S. school children — and is doubling every 3 to 4 years! Children with ADHD often continue the symptoms into adulthood. In 1997, somewhere between 6.5 million and 9 million adults in the U.S. were estimated to have ADHD, which makes it as large a problem as clinical depression or drug abuse. Ritalin Needs More Testing A 1995 study conducted by the federal government's National Toxicology Program (NTP) found that Ritalin caused liver tumors in mice. "The NTP study sends a strong warning that Ritalin may cause cancer — in the liver or other organs — in humans," says Samuel Epstein, professor of occupational and environmental health at the School of Public Health, University of Illinois Medical Center. "Millions of young children take Ritalin for long periods of time, and children may be especially vulnerable. It would be prudent for HHS [U.S. Department of Health and Human Services] to discourage doctors from prescribing Ritalin, especially in the absence of an explicit warning about the cancer risk." Epstein and several other cancer specialists — including Emmanuel Farber at the University of South Carolina School of Medicine, Marvin Legator at the University of Texas Medical Branch at San Antonio, and Richard Clapp of Boston University — have urged HHS to sponsor new animal and human studies on Ritalin and other stimulant drugs. "It makes a lot more sense to try modifying a child's diet before treating him or her with a stimulant drug," said Dr. Marvin Boris, a pediatrician in Woodbury, New York, whose 1994 study found that diet affected the behavior of two-thirds of his subjects. "Health organizations and professionals should recognize that avoiding certain foods and additives can greatly benefit some troubled children." What's Diet Got to Do with It? That food allergies are associated with ADHD is nothing new. In the preface to his book, Thom Hartmann mentions the pioneering work done more than twenty years ago by the pediatric allergist Dr. Ben Feingold. He discovered that children with skin disorders were allergic to certain foods or additives, particularly aspirin-like compounds called salicylates. When these were removed from the children's diet their skin problems cleared up, but also their behavior changed. Many of these kids had been diagnosed with hyperactivity. Without the allergens in their diets, the hyperactivity was dramatically reduced or quite often disappeared. After reviewing 23 scientific studies, the CSPI report contends that food dyes and certain foods can adversely affect children's behavior. It cites 16 controlled studies over the past 25 years which found that food additives exacerbate the symptoms of ADHD in some children. A 1976 study of U.S. children aged 6 to 11 found they ingested an average of 76 milligrams of food dyes per day, and ten percent ingested twice that amount. (Since then, the quantity of food dyes manufactured per person in the U.S. has increased 50%.) Government Urged to Advise Caution and Conduct More Studies The CSPI and several experts on diet and behavior have asked the Department of Health and Human Services to undertake new research into the link between diet and behavior and to "consider banning synthetic dyes in foods and other products (such as cupcakes, candies, sugary breakfast cereals, vitamin pills, drugs, and toothpaste) widely consumed by children." "The Department of Health and Human Services should withdraw its printed and Internet documents that largely dismiss the effect of food ingredients on behavior," said Michael F. Jacobson, executive director of CSPI and lead author of the report. "The FDA should halt distribution of a pamphlet on food additives that it co-published with an industry group." The pamphlet titled "Food Color Facts" was actually written by the International Food Information Council. This trade association represents makers of food additives including General Mills, Kraft, Procter and Gamble, Pepsi-Cola, Coca Cola, Monsanto (maker of aspartame), and Ajinomoto (maker of monosodium glutamate). It states that "there is no evidence that food color additives cause hyperactivity or learning disabilities in children." It ignored the 16 double-blind studies cited by CSPI which showed that food dyes do worsen the symptoms of ADHD in some children. The CSPI report also concluded that poor diet undoubtedly contributes to ADHD. Large numbers of U.S. children are considered malnourished, because they receive less than 60% of the recommended daily allowances (RDA) for a particular nutrient — an amount needed to avoid disease, not to function optimally. Chemicals and Behavior In a Rachel's Environment & Health Weekly report on "ADHD and Children's Environment," Peter Montague points to the role of prenatal exposures to lead, cigarette byproducts, alcohol, and pesticides as well as exposure to low levels of industrial chemicals that may interfere with hormones, especially thyroid hormones. Previous studies have shown that combinations of chemicals can increase the toxicity of a single poison by a factor of 160 to 1600. (Science, June 7, 1996) Montague concludes: "At a time when Americans are searching for causes of aggression and violence among children, it would make sense to consider malnutrition, food additives, tobacco additives, toxic metals, pesticides and other endocrine-disrupting industrial toxicants — all of which many U.S. children are exposed to from the moment of conception onward." Why Has Nutrition Become Alternative Medicine? During the second half of the twentieth century, commercial interests have succeeded in changing the popular meaning of "primary" healthcare. Common sense nutritional approaches to health are now labeled "alternative" or "complementary." Drugs have become primary. Throughout history, healers have said that food is the best medicine. A child's mental health and behavior are intimately related to what he eats — both the good and the bad. Is he getting enough essential macro and micronutrients? Is he consuming too many non-foods and toxins? How can there not be mental disorder when potato chips and French fries make up more than one-quarter of the vegetable servings eaten by children, and nearly one-third of the veggies eaten by teenagers? How can a child function at his best when he drinks more soda pop than water? This is common sense, but the commercial media does not remind us of this. Because vitamins, minerals, and other nutrients are not patentable, there is little commercial incentive to promote them. Dr. Joseph M. Mercola, D.O., the medical director of the Optimal Wellness Center in Schaumburg, Illinois, treats complex chronic illness by integrating lifestyle changes with innovative tools in nutrition and energy medicine. Writing in his December 1999 column in the Townsend Letter for Doctors & Patients, he's says that "restricting sugar, grains and all fluids but water will improve nearly all children with ADHD. Nothing works all the time, but this is close to it." Dopamine and Attention Charles Gant, M.D., Ph.D., a New York physician believes ADD/ADHD is likely caused by an imbalance in dopamine. This vital neurotransmitter helps integrate thoughts, feelings, and sensory information in the frontal lobes, as well as update feedback about current motor activity. He elaborates: "In evolutionary terms, this is the last part of the human brain to develop and is one of the first parts to lose its function when there is a generalized stress or injury to the central nervous system. Because this recent brain structure has not had the benefit of millions of extra years of 'road testing,' that the older, more rugged parts of the brain have had, it is more vulnerable to modern-era stress, neurotoxins, and nutritional deficiencies." When dopamine activity is compromised, Gant says people become unfocused and distractible because they have difficulty coordinating all this information and choosing the next task to attain. This fits in with a growing body of evidence that implicates one region of the brain as causing ADHD. A study presented at the May 1999 meeting of the American Academy of Neurology found that ADHD children possessed less gray matter in both frontal lobes, with the right frontal lobe averaging about 5% less fewer cells. ADHD children cannot stop themselves from responding to every stimulus. Damaged or underdeveloped cellular circuits in the frontal lobes may be a structural reason why these children have difficulty staying on task. Dopamine is made from two essential amino acids, tyrosine or phenylalanine, in the presence of adequate amounts of folic acid, iron, vitamins C, B3 and B6. Therefore it could be a dietary deficiency of these necessary nutrients that is causing the dopamine deficiency, says Dr. Gant. He has found that ADD can be treated with nutrients and amino acids, the raw materials the brain uses naturally to synthesize this neurotransmitter. "Nutritional supplementation will virtually erase symptoms of garden variety, uncomplicated ADD." Sources of tyrosine include almonds, avocados, bananas, dairy products, lima beans, pumpkin seeds, and sesame seeds. MAGNESIUM Deficiency in another essential nutrient, magnesium, may be the basis of ADD — as well as numerous other disorders of the brain and body. This should not be too surprising. Vitamins themselves were originally discovered during the search for the cause of beriberi, a life-threatening degeneration of the nerves. Thiamine was identified as the nutrient missing from polished rice. It became the first vitamin, B1, and was called the "nerve vitamin." We now know that thiamine is necessary for proper functioning of the nervous system and good mental health. Among other things, it is needed to create myelin, the protective sheath that insulates nerve fibers. Even a mild B1 deficiency can cause nerves to become hypersensitive and an individual to become irritable, apathetic, and forgetful. The Mineral that Matters Although magnesium is fundamental to brain health and fitness, this essential mineral has not been given the respect it deserves. The vast majority of people do not get even the minimum recommended daily amount of magnesium, and most are unaware of magnesium's vital role in the human body. (Again, there is no financial incentive to promote magnesium.) In the cerebrospinal fluid that bathes the brain and spinal cord, magnesium is present in higher concentrations than in the blood plasma. More than 300 different enzymes in the human body require magnesium to function, and many are crucial to cerebral metabolism and cognitive function. For example, magnesium is needed by the enzymes that participate in the conversion of dietary sugars and fats into energy. Magnesium is essential to the production, storage, and utilization of ATP, the body's primary molecular form of energy. Proper brain function depends on a constant supply of this biochemical energy. When magnesium is depleted or chronically deficient, then brain metabolism and brain power suffer. The ability to pay attention and maintain focus is compromised. Magnesium and Attention-Deficits Biochemist James South, M.A., a leading expert on brain nutrition, has noted a remarkable similarity between the symptoms of ADD and the symptoms of chronic magnesium deficiency. These include difficulty concentrating and remembering, confusion and disorientation, irritability and apathy, and muscular restlessness. He points out magnesium's many roles in mental function. Because magnesium controls the rate of synaptic activity between neurons, low levels of magnesium may cause nerves to fire too easily — even from minor stimuli. South says this can result in noises sounding excessively loud, lights seeming too bright, and emotional reactions becoming exaggerated. The brain may even be too stimulated to sleep. At neuromuscular junctions, calcium allows muscles to contract, however to relax they need magnesium. Chronic magnesium deficiency can therefore lead to excessive muscle tension, including spasms, twitches, and restlessness. South notes that this can be especially true of the hands, feet, and facial muscles — and that one of the main criterion for diagnosing hyperactivity listed in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders IV is: "often fidgeting with hands or feet, or squirming in a seat." This is often the only way a child can prevent magnesium-deficient muscles from cramping or spasming. Magnesium is needed by the enzyme that allows cells to dispose of ammonia, an extremely toxic byproduct of normal protein metabolism. The ability to focus and pay attention can be compromised by even small increases in brain ammonia. Magnesium is crucial to the synthesis of the DNA, RNA, and the brain proteins required to form and store memories. A chronic magnesium deficiency could limit the ability of brain cells to network, especially in the most formative years of childhood. Magnesium and Essential Fatty Acids Magnesium activates D6D, the enzyme that converts dietary essential fatty acids (EFAs) into DHA and other long-chain fatty acids that are vital structural components of brain cell membranes and essential for proper mental function. Prostaglandins are also synthesized in this pathway. These hormone-like substances regulate metabolic functions within cells, including inflammatory processes. Several recent research projects have highlighted the connection between EFAs and learning disorders. Dr. Laura Stevens and her colleagues at Purdue University found that many hyperactive children are deficient in EFAs. Although they consumed plenty of EFAs in their diet, the hyperactive boys in their study were less able to convert the dietary EFAs into the long chain derivatives, DHA and AA, which require the active enzyme D6D. Research conducted by John R. Burgess, Ph.D., of Purdue University's Department of Foods and Nutrition, indicates that deficient levels of DHA are also correlated with behavioral problems in children. Burgess studied a population of children in Indiana and found that subjects with ADHD had significantly lower levels of DHA when compared to controls. Stress Depletes Magnesium In preparation for "fight or flight," one of the actions of stress hormones is to take magnesium out of muscle cells and replace it with calcium. This gives muscles the needed rigidity to defend against a foe, however, it can also lead to cramps or spasms — even a heart attack. And, the magnesium that leaves does not necessarily reenter the muscle cells once the stress is over. A 1994 review of more than 250 references found that magnesium deficiency enhances stress reactions. In the authors' words: "Stress intensifies release of catecholamines and corticosteroids. . . . When magnesium (Mg) deficiency exists, stress paradoxically increases risk of cardiovascular damage including hypertension, cerebrovascular and coronary constriction. . . . Dietary imbalances such as high intakes of fat and/or calcium (Ca) can intensify Mg inadequacy, especially under conditions of stress. . . . A low Mg/Ca ratio increases release of catecholamines, which lowers tissue (i.e. myocardial) Mg levels. . . . Thus, stress, whether physical (i.e. exertion, heat, cold, trauma, burns), or emotional (i.e. pain, anxiety, excitement or depression) and dyspnea as in asthma increases need for Mg. Genetic differences in Mg utilization may account for differences in vulnerability to Mg deficiency and differences in body responses to stress." (J Am Coll Nut, Oct. 1994) What's Heart-Smart is Also Brain-Gain The heart muscles of cardiac arrest victims typically have a 20% lower magnesium level than those who died from causes unrelated to the heart. According to the U.S. National Academy of Sciences, more than 50 studies, in nine countries, have indicated an inverse relationship between water hardness and mortality from cardiovascular disease. People who drink water that's deficient in magnesium and calcium generally appear more susceptible to this disease. A 1977 report by the Academy's Safe Drinking Water Committee estimated that a nationwide initiative to add calcium and magnesium to soft water might reduce the annual cardiovascular death rate in the United States by 150,000. We now know that what's good for the heart is even better for the brain, therefore the importance of magnesium to mental health, from ADD to AD, becomes paramount. Low magnesium levels in the brain make cerebral vessels more prone to constriction, and even to spasm — a cause of stroke. What's more, research has shown an association between low magnesium levels in the brain and increased uptake of aluminum, a toxic metal implicated in dementia. (Fluoride has also been shown to increase the uptake of aluminum. Both of these chemicals are added to most water supplies.) Why the Deficiency in Magnesium? Several factors contribute to the lack of magnesium in our diet. First of all, our soils are often depleted of magnesium. Then, food processing and cooking destroy the magnesium that's in the food. Fats, meats, and dairy products — a big part of the American diet — are low in magnesium. Furthermore, the magnesium that is consumed may not be digested. Intestinal absorption of magnesium is easily compromised, especially by high dietary and supplementary intakes of calcium. Both minerals compete for the same intestinal absorption sites, with calcium given priority. Excessive vitamin D (from milk and multivitamins) can also impair magnesium status. James South notes that "the typical American high-dairy diet contains 2.5 to 4 times as much calcium as magnesium! Many physicians ill-advisedly recommend that children (because of their growing bones) and adults (because of osteoporosis fears) take 500 to 2000 mg of calcium supplements daily!" Many factors, particularly stress (including physical stress from overexercising), increase magnesium loss from the body. Of all the drugs known to deplete magnesium, alcohol is the most notorious. Soft Drinks are Hard on the Brain The high levels of phosphoric acid in soft drinks can combine with magnesium and calcium in the gut to form mineral phosphates that are lost in the feces. Sugar is a powerful urinary magnesium "spiller." Acidic sodas in aluminum cans can leach the toxic metal into the liquid, which is amplified if the soda was made from water that contained silicofluorides, the chemicals most commonly used to fluoridate drinking water. At a fundamental level, drinking soda pop decreases the amount of pure water a child gets, which can lead to dehydration which depletes the brain and other organs of fluids. (The brain is more than 75% water.) ADHD Children Found Deficient in Magnesium In a 1997 study, Polish researchers found that 95% of the ADHD children they examined were deficient in magnesium. About half of these children were assigned to a six-month trial of magnesium supplementation (200 mg/day). "At the end of the trial, the children whose treatment included magnesium supplements showed significant reductions in parent and teacher ratings of ADHD symptoms compared to the children who had not received the supplements." (Magnesium Research 10, 1997) What to Do? Supplement. South concludes: "Given this overlap of magnesium deficiency and ADD symptoms, and given the woefully inadequate magnesium status of the American diet and way of life, I suspect the vast majority of ADD sufferers are magnesium deficient. I also believe this deficiency is a major contributing cause, if not the primary cause, of most ADD cases." Many nutritionists believe the optimum intake of magnesium — especially when stress is a factor — should be two to three times higher than what Americans are typically getting from their diet. Supplements are the easiest way to increase magnesium intake. Good forms of magnesium that are well-absorbed and well-utilized include magnesium ascorbate, aspartate, chloride, citrate, glycinate, succinate, and taurinate. Forms that are not so well absorbed are magnesium oxide and carbonate. Although the main side effect of excess magnesium is diarrhea, it's wise to check with a health professional who is knowledgeable about nutrition before supplementing. (Because magnesium chloride can irritate sensitive stomachs, it should never be taken on an empty stomach.) Zinc About It Magnesium is not the only mineral associated with attention deficits. Insufficient levels of zinc have been found in children with lowered learning ability, apathy, lethargy, and mental retardation. Hyperactive children may be deficient in zinc and vitamin B-6 and have an excess of lead and copper. (Biol Psychiatry, April 1982) The highest levels of zinc are found in synapses and in the hippocampus, the area of the brain vital to memory formation and sensory integration. Zinc is stored with histamine in hippocampus, where it prevents excessive histamine release, which severe allergy-suffers experience as a spacey, foggy feeling that makes it difficult for them to focus their attention. Like magnesium, zinc is also needed to synthesize DHA and the other long-chain fatty acids and prostaglandins that the brain requires for optimal functioning. TELEVISION An obvious modern "environmental" factor that affects behavior and influences the mind is television. A 1999 study by the Kaiser Family Foundation found that typical American children aged 2 to 18 "consume" media (mainly TV, but also computers and music) for more than five hours a day — usually alone in their room. Kids older than seven are putting in seven-hour days in front of the tube! TV Contributes to Stress and Loneliness Children who watch a lot of TV alone are less able to cope with stressful situations. They don't develop relationships with other children and do not learn to deal with stress, according to Michele Cooley-Quille, a professor of mental hygiene at Johns Hopkins School of Public Health. TV offers a "false sense of interpersonal relations," she says. Children feel they have relationships with TV characters, but this illusion robs them of the emotional and intellectual benefits of real social interaction and contributes to a pervasive sense of loneliness. Because the influence of mass media is becoming a major public health concern, the American Academy of Pediatrics now recommends that children should not have television sets in their bedrooms, and that children less than two years old not watch any television at all. Furthermore, the Academy says parents should fill out a "media history" along with a medical history of their child when consulting their pediatrician. The content of television is obviously a huge factor that influences behavior — and the subject of much debate — but it is the medium itself that aggravates attention problems, as Jerry Mander thoroughly explains in his classic 1978 book, Four Arguments for the Elimination of Television. With images that quickly change every few seconds or less, TV entrains brains to constantly change focus. No wonder people are have trouble paying attention to single thing for any length of time. Television Teases the Senses In his 1991 follow-up book, In the Absence of the Sacred, Mander describes television as a kind of sensory tease that has become a major cause of hyperactivity. He refers to the research of Australian psychologists Merrelyn and Fred Emery who have investigated the correlation between increases in TV viewing and hyperactivity in children. Mander explains how the unused physical energy created by television images eventually bursts out in aimless, random, speedy activity. "While sitting quietly in front of the TV, the child sees people punching each other on the screen. There is the impulse to react — the fight-or-flight instinct is activated — but since it would be absurd to react to a television fight, the child suppresses the emotion. As the fighting continues, so does the cycle of impulse and suppression. Throughout the television-viewing experience, the child is drawn back and forth on the see-saw of action and suppression, all the while appearing zapped and inactive. When the set goes off, this stored-up energy bursts forth in the disorganized, frantic behavior that we associate with hyperactivity. Often, the only calming act is to again put the set on, which starts the cycle anew." Two years after television was introduced to a native village in the Northwest Territories of Canada, teachers found that the children were restless and hyper, their attention span was much shorter than before television, and they had just about given up reading. Television Accelerates the Pace of Life Mander says that television, combined with video games and computer fixation, is producing generations of people moving so quickly that they cannot attune themselves to slower, natural, primordial rhythms. "The natural world is really slow. Save for the waving of trees in the wind, or the occasional animal movement, things barely happen at all. To experience nature, to feel its subtleties, requires human perceptual ability that is capable of slowness. It requires that human beings approach the experience with patience and calm. Life in the modern world does not encourage that; it encourages the opposite. . . . We live in a world of constant catharsis, constant change, constant unrest. While out in the real world, in nature, we become anxious and uncomfortable. We desire to get back indoors, to get that TV set back on, to get 'up to speed.' "For children, this change is very serious, and has been well noted by educators. Countless teachers have told me how young people are utterly unable to maintain focus. They become bored after only a few minutes of the same subject. They need constant change." TV's Distorted Reality is Dangerous A 1998 study by Spanish researchers at the University of Granada found that the more time children spent watching TV, the greater their risk of injury — even more so than children who played potentially dangerous sports. TV makes children believe that harmful actions are without consequences. Lead researcher Dr. Jose Uberos said that children who watch TV excessively "receive a greater number of distorted messages about reality that become converted into false real-life experiences and distort the child's adaptation to his or her surrounding environment." Nature Nurtures the Human Brain In Sibling Society, author and poet Robert Bly describes the vital role of the natural environment to the proper development of the neocortex (or cortex), that part of our brain that makes us human. Instead of relying on instinctual reactions, the neocortex must learn to behave. That's why we're so uniquely curious. In the words of Konrad Lorenz: "Human exploratory inquisitive behavior — restricted in animals to a brief developmental phase — is extended until the onset of senility." But in order to learn, children must interact with the nature. And that's the problem today, says Bly: "The frightening thing, for us in the industrial world, is that the neocortex may not reach its maturity — and the human being with it — unless it wraps itself intricately, intensely, in the sense world, and draws the sense world in around it, seeing, smelling, hearing, touching, weighing, tasting. . . . The hours and hours that children, until the last few years, spent playing outdoors are hours in which the brain receives the food it wants." Television Denatures Children Television steals this observation time and gives little in return, Bly insists. We do not immerse ourselves in the details of nature. The thousands of hours of playtime children lose to television is a serious and irrevocable loss to the neocortex. When the neocortex no longer interacts with plants and animals but only plays with its own inventions, a truly new element has entered human life. "The neocortex becomes analytical about analysis, or inquisitive about inquisitiveness." We no longer receive or learn to give the years of nourishment and protection needed for growth and learning. Immediacy replaces the "hard work of figuring out how to give delight and entertainment to ourselves and others." Bly concludes that if the "brain cannot do its work, which is to study animals, wind, thunder, stones, and feathers in detail, it cannot feel safe. Not feeling safe, the boy or girl feels utterly unable to confront the 'ills that flesh is heir to,' and finds a way to numb the fearful mind and the emotions." Illuminating the Problem The human brain is a product of its environment. To decipher attention-deficit problems, one must consider all sources of information received by the brain, especially the most fundamental ones — for example, light. Light has an enormous effect on health, something that scientists are only beginning to recognize. Recently, night-time light in infants' bedrooms has been linked to nearsightedness later in life. This century, we have significantly altered the quality of light under which we work and study. Most of us know how tiring fluorescent lights can be, but this "malillumination" is more than annoying; it is a very real problem. Your eyes are actually extensions of your brain and are the portal of entry for approximately 90% of the information you receive in a lifetime. Cool-white fluorescent lights produce a rather distorted spectrum of light that is deficient in the red and the blue-violet areas of the spectrum — precisely where the sun's emissions are the strongest. Research presented by Jacob Liberman, O.D., Ph.D., in his eye-opening 1991 book, Light: Medicine of the Future, clearly shows that the cool-white fluorescent lighting used in most classrooms creates bodily stress and thus interferes with learning ability. Lights Affect Students' Learning Ability and Behavior In Dr. John Ott's 1973 study involving four first-grade classrooms in Sarasota, Florida, full-spectrum fluorescent lights that more closely simulated sunlight were installed in two of the four windowless rooms. Cool-whites were in the other two. The results were significant: "Under the cool-white fluorescent lighting, some students demonstrated hyperactivity, fatigue, irritability, and attentional deficits. In the classrooms with full-spectrum lighting, however, behavior and classroom performance as well as overall academic achievement improved markedly within one month after the new lights were installed. Furthermore, several learning-disabled children with extreme hyperactivity problems miraculously calmed down and seemed to overcome some of their learning and reading problems while in classrooms with full-spectrum lighting." Creatures of Habitat As the adapted offspring of Earth, we are inseparable from our environment. Our brain chemicals and cerebral circuitry reflect what we eat and how we learn. A lifetime of nutritional and sensory input influences our thought processes and behavior — leading to the habits that shape our personality and form our character. It is in the details of daily life that we are likely to discover the way out of the attention-deficit dilemma. Topgraphic Mapping of Brain with Food Induced Attention Deficit Disorder Uhlig T, Merkenschlager A, Brandmaier R, Egger J. Institute for Child Health Research, Clinical Sciences Division, West Perth, Australia. In 15 children suffering from food induced attention deficit hyperkinetic syndrome, topographic EEG mapping of brain electrical activity was carried out following avoidance and ingestion of previously identified provoking foods. A crossover design was used and recordings were interpreted independently by two investigators, one of whom was blind to the order of testing. During consumption of provoking foods there was a significant increase in betal activity in the frontotemporal areas of the brain. This investigation is the first one to show an association between brain electrical activity and intake of provoking foods in children with food-induced attention deficit hyperactivity disorder. CONCLUSIONS: These data support the hypothesis that in a subgroup of children with attention deficit hyperactivity disorder certain foods may not only influence clinical symptoms but may also alter brain electrical activity. The clinical role of computerized EEG in the evaluation and treatment of learning and attention disorders in children and adolescents. Chabot RJ, di Michele F, Prichep L, John ER. Department of Psychiatry, Brain Resarch Laboratories, New York University School of Medicine, NY, USA. bob@br14.med.nyu.edu Quantitative EEG (QEEG) can play an important role in the evaluation and treatment of children and adolescents with attention deficit and learning disorders. Children with learning disorders are a heterogeneous population with QEEG abnormality in 25% to 45% of reported cases. EEG slowing is the most common abnormal finding, and the nature of the QEEG abnormality may be related to future academic performance. Children with attention disorders are a more homogeneous population, with QEEG abnormalities in up to 80%. In this population, frontal/polar regions are most likely to show deviations from normal development, with the thalamocortical and/or septal-hippocampal pathways most likely to be disturbed. QEEG shows high sensitivity and specificity for distinguishing normal children and children with learning disorders and attention disorders from each other and may provide useful information for determining the likelihood that children with attention problems will respond to treatment with stimulant medication.

ALLERGY NEWS

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Genetic and Environmental Factors Trigger Allergy NEW YORK (Reuters Health) The presence of common gene mutations can increase the allergic response in sensitive patients who are exposed to diesel exhaust, investigators in California report in The Lancet. While these findings explain why some individuals are more susceptible to the effects of air pollution, they also suggest that antioxidants, such as vitamins A, E and C, may prevent the effects that air pollution have on allergic inflammation, lead investigator Dr. Frank D. Gilliland told Reuters Health. Gilliland of the University of Southern California in Los Angeles and his colleagues examined genes that encode for glutathione-S- transferases (GSTs), enzymes that metabolize reactive oxygen species and detoxify chemicals present in diesel exhaust. Mutations of these genes, which occur in up to 20 percent of the general population, are associated with airway hyperresponsiveness and asthma. To investigate the mechanism driving the effects of air pollution on allergic responses, Gilliland's group evaluated GST genes in 19 patients who were allergic to ragweed and had a history of allergic rhinitis. The subjects with GST mutations had significantly higher levels of nasal IgE and histamine -- markers of allergic response -- to diesel exhaust particles than to the allergen alone. In the subjects with the most GST mutations, "diesel exhaust had a huge adjuvant effect on the allergic response to allergens," increasing response up to 20 times greater than allergen exposure alone, Gilliland said. In the past, the presence of these GST mutations would not have made much difference to human health, he explained. "But now that we have new and increasing levels of pollutants, that's at least partially what is bringing on some of the increases in allergy susceptibility." He noted that in some populations, 50 percent to 60 percent of individuals have allergies, "and that's very different from what it was 50 or 100 years ago." "We now have ways to identify individuals susceptible to air pollution, and, because this sensitivity seems to be regulated by genetic and dietary factors, new approaches are emerging that might help protect these individuals from ambient pollution," Drs. F. J. Kelly and Thomas Sandstrom remark in a related commentary. Kelly is on staff at King's College in London, and Sandstrom is at University Hospital, Umea, Sweden. Oral food challenge increases in vitro IL-4 production by peripheral blood mononuclear cells in allergic patients. Andre F, Andre C, Cavagna S. Laboratoire d'Immunopathologie Digestive, INSERM, Centre Hospitalier Lyon-Sud, Pierre-Benite, France. The aim of this study was to investigate interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) production by peripheral blood mononuclear cells (PBMC) in response to oral challenge in patients with food allergy. Thirty-one patients were compared with 10 healthy subjects. Cell cultures were prepared before and 150 min after single-blind, placebo-controlled, oral food challenge. In vitro production of cytokines was observed after stimulation with phytohemagglutinin (PHA) plus phorbol myristate acetate (PMA). Patients were characterized according to their reactions. In vitro IL-4 production was significantly greater in patients with food sensitization than in controls. The 18 patients with positive food challenge presented significantly greater IL-4 production after food challenge than before. IFN-gamma production was not modified. In the 10 control subjects and in 13 patients with negative food challenge, IL-4 and IFN-gamma production was comparable before and after food challenge. The increased IL-4 production in patients with positive oral food challenge could account for the development of polysensitization. This situation might be relevant to other allergic diseases and to treatments. Measurement of intestinal permeability to mannitol and lactulose as a means of diagnosing food allergy and evaluating therapeutic effectiveness of disodium cromoglycate. Andre C, Andre F, Colin L, Cavagna S. Laboratoire d'Immunopathologie Digestive INSERM, Centre Hospitalier Lyon Sud, Pierre-Benite, France. Gastrointestinal permeability was evaluated in 90 fasting healthy subjects and 60 patients with food allergy by oral administration to both groups of 5 g of mannitol, a marker of absorption of small molecules, and 5 g of lactulose, a marker of abnormal absorption of large molecules, and subsequent measurement of urinary excretion of mannitol and lactulose. In healthy subjects, mean 5-hour urinary excretion of mannitol was 14.11% and of lactulose 0.26%. In the fasting state, the 60 patients with food allergy exhibited a mean urinary recovery of mannitol of 13.22%, not significantly different from that in healthy subjects. Mean recovery of lactulose in the patients with food allergy was 0.55%, significantly greater than in the healthy patients. After ingestion of food allergens by the patients, mean mannitol recovery fell to 11.57% and mean recovery of lactulose rose to 1.04%, both values being significantly different from those obtained in the fasting patients. On challenging the patients after they had taken sodium cromoglycate, mean mannitol and lactulose recoveries (13.53% and 0.62%, respectively) were not significantly different from those in fasting patients but were significantly different from those obtained on challenging patients unprotected by sodium cromoglycate. Evaluation of intestinal permeability in this way provides an objective means of diagnosing food allergy and assessing the effectiveness of anti-allergic agents such as sodium cromoglycate.

AUDITORY NEWS

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Central Auditory Processing Disorders (CAPD) One Cause of Attention Deficits, Defiance and School Failures. By: Michael G. Conner, Psy.D, Clinical, Medical & Family Psychologist Published in the Family News, 2001 * Does your child have a short attention span? * Do they become stressed or nervous when required to listen? * Are they easily distracted? * Do they become restless or bored in classrooms and group discussions? * Does your child have difficulty following directions? * Do they become defensive or argumentative for no apparent reason? * Do they say, "You don’t understand", even when you do? * Did your child experience a delay or problem in language development? Counselors, mental health professionals and schools most frequently attribute these behaviors to depression, anxiety, attention deficits or an oppositional and defiant disorder. That’s all fine, but the problem may not stop there and the solution may be far from clear. A diagnosis can tell you what type of problem your child may have, but it can tell you very little about the cause or what to do about it. There are many possible reasons, but one reason that some children act this way is called a central auditory processing disorder (CAPD). A central auditory processing disorder is an inability or limited ability to pay attention, recognize, tell the difference, remember or comprehend auditory information. A person with CAPD can have normal intelligence and hearing. Children with normal auditory processing skills are able to understand speech in a wide variety of listening conditions. Symptoms of CAPD include but are not limited to, * an inability to tune out background noise * problems understanding words when there are poor acoustics * an inability to adapt to a wide variety of speaking styles * difficulty understanding incomplete sentences. How Does CAPD Affect Children? We live in a world where children are expected to participate in family life, attend school and socialize with other children and adults. We hope that our children will participate and contribute productively in family life. We expect them to attend school, complete their homework and become involved in community and school activities. All this becomes difficult for children with CAPD. Children with CAPD don’t recognize they have a problem with auditory processing. Children with CAPD do not understand what is being said as well as they should. They don’t learn as well as other kids – especially in large noisy classrooms and homes. They may understand only portions of what is said. They act like they understand but they really become lost when more than one person is talking, there is background noise and people are speaking rapidly with incomplete sentences. Fear and anger during a conversation can make understanding even more difficult. Nearly all these kids lose confidence and end up feeling insecure. Rather than get real help, they repeatedly encounter moments of despair. They feel incapable and unable to change for the better. Some may become isolated, withdrawn and depressed. Others become bored and restless. They can look like they aren’t paying attention or they don’t follow instructions. Rather than feel incompetent and bored, many will become disruptive, risk takers or thrill seekers. A large number will become cynical, argumentative and even aggressive when challenged. How Common is CAPD? What disturbs me the most about these disorders is how often CADP is not identified. Drug companies are quick to encourage parents to treat symptoms (anger, depression, anxiety, attention deficits) with drugs. They ignore dealing with the cause. Family counseling and parent education can help, but it takes time. Very few counselors and teachers have even heard of CAPD. Researchers cannot agree on the number of children affected by this disorder. Many teachers, special education professionals and school psychologists have never heard of it. But the disorder may be as common as reading disorders – referred to as dyslexia. In my practice I have identified 3 out of 20 troubled adolescents with undiagnosed CAPD. Another couldn’t hear well enough to avoid misunderstandings. Partial deafness and auditory processing problems may be more common than we think. What Causes CAPD? CAPD is a neurological problem that may be inherited or caused by a birth defect. There appears to be a link between CAPD and ear infections during infancy. But that link is not entirely clear. We know that ear infections don’t cause CAPD in all children. There may be other contributing factors involved that we don’t understand yet. Does My Child Have CAPD? The diagnosis of CAPD normally involves consultation with a psychologist, an audiologist and a specialist in learning disabilities. A cooperative team approach is best. Screening for CAPD with young children is more complicated and difficult than the evaluation of adolescents and adults. In all cases, a thorough hearing examination is necessary. Standard hearing screenings conducted by public schools are not adequate for a diagnosis of CAPD. I have encountered adolescents who passed a school hearing exam but were later found to be partially deaf. Keep in mind that school based hearing exams are very important. They are screenings and a very important part of your child's education. A screening for CAPD is a specialized activity over and above what schools should be doing. Evaluations of CAPD can be reliably conducted on children who are 8 years and older. Dr. Conner is a clinical, medical and family psychologist who completed a research and training fellowship in graduate medical education and health education. He is Board Certified in Traumatic Stress, Emergency Crisis Intervention and Emergency School Response.. Copyright 2001, Michael G. Conner

AUTISM NEWS

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What is Semantic-pragmatic Disorder? by Julia Muggleton The term 'semantic pragmatic disorder' has been around for nearly l5 years. Originally it was only used to describe children who were not autistic. Features it includes are:- delayed language development learning to talk by memorizing phrases, instead of putting words together freely repeating phrases out of context, especially snippets remembered from television programmes muddling up 'I' and 'you' problems with understanding questions, particularly questions involving 'how' and 'why' difficulty following conversations Children with this disorder have problems understanding the meaning of what other people say, and they do not understand how to use speech appropriately themselves. Soon both research and practical experience yielded two important findings: 1.. Many people who definitely are autistic have this kind of language disorder (Dustin Hoffman's character Raymond in the film 'Rainman' being a typical example). 2.. Most of the children diagnosed as having semantic pragmatic disorder do also have some mild autistic features. For example, they usually have difficulty understanding social situations and expectations, they like to stick fairly rigidly to routines, and they lack imaginative play. For a while some language therapists maintained there was still an important difference between children with semantic pragmatic disorder and children who were truly autistic. They believed the autistic features seen in children with semantic pragmatic disorder were only a result of their difficulty with language. However, further research has shown that there is probably a single underlying cognitive impairment which produces both the autistic features and the semantic pragmatic disorder . The fact that children with semantic pragmatic disorder have problems understanding the meaning and significance of events, as well the meaning and significance of speech, seems to bear this out. Eventually the idea of an autistic continuum was used to explain the situation. All the children on the continuum have semantic pragmatic difficulties, but the degree of their other autistic impairments can be severe or moderate or mild. This parallels the autistic continuum relating Asperger syndrome, where all the children have a marked social impairment but those with Asperger syndrome have only a relatively mild and subtle language impairment. It seems that children who are diagnosed as having a semantic pragmatic disorder might more accurately be described as high-functioning autistic. Clinicians tend to give all autistic children who have good intelligence the label Asperger syndrome, even if a child actually has very limited speech. But there are important differences between bright autistic children with semantic pragmatic difficulties and bright autistic children with Asperger syndrome. Children with semantic pragmatic difficulties have usually learnt to talk late, whereas (according to diagnostic guidelines) children with Asperger syndrome were able to talk in sentences by the age of three. Also children with semantic pragmatic difficulties do better on performance IQ tests than verbal IQ tests, whereas with children with Asperger syndrome the results tend to be the other way round. However, if a child with semantic pragmatic difficulties eventually becomes a fluent talker, the difference between the labels 'high functioning autistic' and ' Asperger syndrome' becomes fairly academic. There is another aspect to the issue of labelling which is altogether more emotive. Many parents feel much more able to cope with the idea of their child having semantic pragmatic language disorder than with the idea of their child being a high functioning autistic. But many other parents find the label semantic pragmatic disorder frustrating and baffling, as they only begin to really understand their child's behaviour when they realise he or she has a form of autism. Yet another issue is the provision of resources. It is a sad truth that many high functioning autistic children are denied the kind of educational language provision they desperately need, purely because of the word 'autism'. These children are more likely to be accepted into language units and schools when they have the label of semantic pragmatic language disorder. Perhaps the only real solution is to educate the educators, so they begin to understand the wide spectrum of autistic disorders, and to forget dated stereotypes. Even better, perhaps they could learn to look beyond the label and to see the child.

BIPOLAR RESEARCH

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Low-field magnetic stimulation in bipolar depression using an MRI-based stimulator. Rohan M, Parow A, Stoll AL, Demopulos C, Friedman S, Dager S, Hennen J, Cohen BM, Renshaw PF. Brain Imaging Center, McLean Hospital, Belmont, MA 02478, USA. OBJECTIVE: Anecdotal reports have suggested mood improvement in patients with bipolar disorder immediately after they underwent an echo-planar magnetic resonance spectroscopic imaging (EP-MRSI) procedure that can be performed within clinical MR system limits. This study evaluated possible mood improvement associated with this procedure. METHOD: The mood states of subjects in an ongoing EP-MRSI study of bipolar disorder were assessed by using the Brief Affect Scale, a structured mood rating scale, immediately before and after an EP-MRSI session. Sham EP-MRSI was administered to a comparison group of subjects with bipolar disorder, and actual EP-MRSI was administered to a comparison group of healthy subjects. The characteristics of the electric fields generated by the EP-MRSI scan were analyzed. RESULTS: Mood improvement was reported by 23 of 30 bipolar disorder subjects who received the actual EP-MRSI examination, by three of 10 bipolar disorder subjects who received sham EP-MRSI, and by four of 14 healthy comparison subjects who received actual EP-MRSI. Significant differences in mood improvement were found between the bipolar disorder subjects who received actual EP-MRSI and those who received sham EP-MRSI, and, among subjects who received actual EP-MRSI, between the healthy subjects and the bipolar disorder subjects and to a lesser extent between the unmedicated bipolar disorder subjects and the bipolar disorder subjects who were taking medication. The electric fields generated by the EP-MRSI scan were smaller (0.7 V/m) than fields used in repetitive transcranial magnetic stimulation (rTMS) treatment of depression (1-500 V/m) and also extended uniformly throughout the head, unlike the highly nonuniform fields used in rTMS. The EP-MRSI waveform, a 1-kHz train of monophasic trapezoidal gradient pulses, differed from that used in rTMS. CONCLUSIONS: These preliminary data suggest that the EP-MRSI scan induces electric fields that are associated with reported mood improvement in subjects with bipolar disorder. The findings are similar to those for rTMS depression treatments, although the waveform used in EP-MRSI differs from that used in rTMS. Further investigation of the mechanism of EP-MRSI is warranted.

BRAIN RESEARCH

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Anterior Cingulate Activity as a Predictor of Degree of Treatment Response in Major Depression: Evidence From Brain Electrical Tomography Analysis Diego Pizzagalli, Ph.D., Roberto D. Pascual-Marqui, Ph.D., Jack B. Nitschke, Ph.D., Terrence R. Oakes, Ph.D., Christine L. Larson, M.S., Heather C. Abercrombie, M.S., Stacey M. Schaefer, M.A., John V. Koger, B.S., Ruth M. Benca, M.D., Ph.D., and Richard J. Davidson, Ph.D.   OBJECTIVE: The anterior cingulate cortex has been implicated in depression. Results are best interpreted by considering anatomic and cytoarchitectonic subdivisions. Evidence suggests depression is characterized by hypoactivity in the dorsal anterior cingulate, whereas hyperactivity in the rostral anterior cingulate is associated with good response to treatment. The authors tested the hypothesis that activity in the rostral anterior cingulate during the depressed state has prognostic value for the degree of eventual response to treatment. Whereas prior studies used hemodynamic imaging, this investigation used EEG. METHOD: The authors recorded 28-channel EEG data for 18 unmedicated patients with major depression and 18 matched comparison subjects. Clinical outcome was assessed after nortriptyline treatment. Of the 18 depressed patients, 16 were considered responders 4–6 months after initial assessment. A median split was used to classify response, and the pretreatment EEG data of patients showing better (N=9) and worse (N=9) responses were analyzed with low-resolution electromagnetic tomography, a new method to compute three-dimensional cortical current density for given EEG frequency bands according to a Talairach brain atlas. RESULTS: The patients with better responses showed hyperactivity (higher theta activity) in the rostral anterior cingulate (Brodmann’s area 24/32). Follow-up analyses demonstrated the specificity of this finding, which was not confounded by age or pretreatment depression severity. CONCLUSIONS: These results, based on electrophysiological imaging, not only support hemodynamic findings implicating activation of the anterior cingulate as a predictor of response in depression, but they also suggest that differential activity in the rostral anterior cingulate is associated with gradations of response. Learning How To Use the Brain Ronald Kotulak Science Writer Chicago Tribune Why are IQ levels rising throughout the developed world? In the U.S., for instance, the average IQ has climbed 24 points since 1918. Similar increases were registered in other countries. We like to think of ourselves as the top of the line, the epitome of a long lineage of human beings. But we still have a lot to learn about our brains and our bodies. Not too long ago breaking the four minute mile was thought to be impossible. But once that barrier was breached by Roger Bannister in 1954, it set the stage for the rise of the superathlete. Today runners routinely run a mile in less than four minutes and every Olympics sees old records smashed. A similar phenomenon is happening to the brain. Not too long ago the brain was considered to be hard-wired. For the most part, people were not concerned about the development of a child's brain until he or she went off to school. Scientists are finding that this notion is as much of a myth as the unbreakable four-minute mile. There is a growing recognition today that the kind of experiences the brain is exposed to in the first three years dramatically influence how it operates-for the rest of its life. Some revolutions are obvious because they are fought with weapons. Others, especially those that require new ways of thinking, tend to sneak up on us. The revolution in brain research is only now revealing itself. For the past 5 to 10 years scientists have been busy figuring out how the brain gets built, how it gets damaged and how it can be repaired. At the core of this new knowledge is the plasticity factor, a term that scientists use to describe the brains amazing ability to constantly change its structure and function in response to experiences coming in from the outside. They recently discovered chemical lifesavers inside the brain called neurotrophic factors, which are critical for the development and maintenance of brain cells. Scientists are searching for ways to replenish these vital chemicals when they decline with age. With the growing understanding of how the brain works comes the opportunity to increase brain power. Who wouldn't want to improve their memory, stop forgetfulness and prevent Alzheimer's disease and other neurodegenerative disorders. For me this is the best time to be a science writer because the powerful new tools of molecular biology and genetic engineering are revolutionizing most fields. Look what's happened to cancer. Ten or so years ago cancer was thought to be more than 100 different diseases and scientists didn't' t think they would ever understand it. But, using molecular biology's new tools, they have solved cancer's mystery. Cancer is a derangement of normal genes. In a sense, we all carry the seeds of our own cancers in our genetic codes. How does that happen? Genes that promote cell division can cause cancer when they forget to turn off. They are like accelerators stuck to the floor. But cancers can also result when the brakes fail, as when genes that are supposed to regulate cell division fall asleep on the job. Turning those same tools loose in neuroscience is producing a similar revolution. Scientists have learned more about the brain in the past 5 years than in the last 100. The explosion of new knowledge has led scientists to a greater understanding of the brain's biology and to finding potential causes of violence. What we thought we knew about the relationship between a deprived or bad upbringing and the increased risk of criminal behavior is now being traced to the brain's chemistry. It is the biological smoking gun of violence. We are now finding the molecular answers to the things that happen to the brain that we could only grope for with older techniques - such as psychology, psychiatry, and sociology. Now we can see thoughts with new imaging devices that can spy on the living, working brain, and we can eavesdrop on individual brain cells to listen to their chatter. With this new technology we can begin to understand through genes, chemistry and experience the sayings, which were based only on observation, "the child is father to the man" and "as the twig is bent, so grows the tree." It also is evident now why a child can easily learn a new language in a foreign country, if he or she does so at the age when the brain cells that process language are being wired. And this new knowledge puts to rest the old, contrived argument of which is more important, nature or nurture, genes or environment. Do we come into the world fully programmed to act the way we do or are we blank slates waiting to be written upon? The answer is that genes and environment are probably equally important. The environment affects how genes work and genes determine how the environment is interpreted. Most people are delighted with all the new information about the organ that is most curious to us. But some don't believe it and others are afraid of it, convinced that such research is a plot to discriminate against some groups, or gain mind control over others. I suppose it is somewhat disconcerting to realize that our thoughts are created by molecules and that the molecules are manipulated by our experiences. But, instead of being limiting, or threatening, I believe the new knowledge about the brain is enlightening and liberating. My foray into this revolution began in 1992 when then editor of The Chicago Tribune, Jack Fuller, was getting ready to launch a year-long project called "Killing Our Children." He asked if there was anything going on in brain research that might be helpful. For me that was like being given the keys to the candy store. As I began to dig in, what initially turned me on was the work of the University of Chicago's Peter Huttenlocher. He was, for the first time, counting synapses, the telephone lines that enable brain cells to communicate with each other. These connections are so small and so numerous that they had previously defied a scientific census. From autopsies of the brains of fetuses and people ranging in age from a few months to their nineties, he took samples about the size of the head of a pin, each containing about 70,000 brain cells. In a sample from a 28-week-old fetus he found 124 million connections between the cells. The same size sample in a newborn had 253 million synaptic connections and in an 8 month old the number exploded to 572 million. At the fastest rate, connections were being built at the incredible speed of 3 billion a second, eventually reaching a total of about 1,000 trillion connections in the whole brain. After that point, the connections begin a gradual decline. By about age 10 or so, half the connections have died off, leaving about 500 trillion, a number that remains fairly constant through most of life. Obviously something pretty terrific was going on. I then became curious about what was happening to the brain cells themselves. I learned that scientists had found a similar explosion there, but it occurred during fetal development. From conception to about halfway through fetal life, brain cells grow from one to about 200 billion. Then brain cells begin to die off, leveling off at about 100 billion at birth, the number that remain through adulthood. Again, something amazing was happening. Both phenomena were examples of genetic frugality. Humans do not contain anywhere near enough genes to make a fully operational brain at birth. So they are given an overabundance of the same or similar cells and connections between them and the brain then has to learn how to make itself work. A surplus of brain cells makes sure that there are enough available for the awakening body to plug into to make the heartbeat, muscles twitch, lungs breathe and eyes move. Brain cells compete for the jobs. It's as if they all come out of the same mold but have to learn different jobs, depending on where they find themselves. Those cells that don't connect die off. There is some thought that the extra cells also give the brain the ability to evolve new capacities, such as language and abstract thinking. A similar thing happens to the synaptic connections after birth. Twice as many are made to guarantee that a newborn will be able to receive input from any environment it is born into, whether it's Chicago or Calcutta, and to adapt to the food, language and culture. The outside world shapes the brain's architecture. The connections that do not become part of this structure perish. The outside world comes in through the senses---vision, hearing, smell, touch, taste---teaching the brain what to become. As I continued my research, other pieces of the puzzle began to fall into place. One was a fairly old piece. In the 70s Torsten Wiesel and David Hubel sewed shut one eye of newborn kittens. Two weeks later the eyes were opened. Although anatomically perfect, the eyes that had been closed could not see. It was the most vivid evidence that there are critical stages of development in which the brain needs the-right kind of outside stimulation to teach brain cells how to do their jobs. In this case it was vision. But it is also true for speech and other functions. During critical developmental periods, brain cells that normally process vision do not learn how to do so if no visual stimuli come in to activate them. They either go off to perform another job, such as helping to process information coming in through the uncovered eye, or they shrivel and die. This discovery had an immediate impact on children who are born with cataracts. Doctors used to wait until the children were older and stronger before removing-the cataracts. They found, to their dismay, that while the children's eyes were perfect, they couldn't see. The same thing that had happened to Wiesel's and Hubel's cats was happening to these children. Learning that early visual stimulation was essential for the cells in the visual cortex to be able to see, surgeons began removing cataracts as soon after birth as possible. Today thousands of children born with cataracts have sight who otherwise wouldn't. That's something to remember when you think about the need for animal research. Another piece of the puzzle was provided by Bill Greenough of the University of Illinois. He exposed one group of rats to a stimulating environment---toys, colors, playmates, exercise devices, challenges. A comparison group of rats was housed in routine laboratory cages with little stimulation. When Greenough looked at the brains of the animals in the two groups he found the key to building brain power. The animals living in the stimulating environment had 25 percent more connections between their brain cells than the control rats, and they were a lot smarter. For a human being, that translates into trillions of extra connections---and remember, connections mean brain power---and possibly a boost in IQ of 20 points or more. What Huttenlocher was seeing in his autopsy studies, and Greenough, Wiesel and Hubel were seeing in animal studies, researcher Harry Chugani was seeing in people. Using PET scans, which can follow the chemistry of thoughts in living brains, Chugani found that the brain is superactive from the ages of 4 to about 10, the years in which brain cells are vigorously learning which connections to keep and which to discard. These are the wonder years of learning, when a child can easily pick up a foreign language without an accent and learn a musical instrument with ease. You can learn a foreign language in adulthood, but it is much harder and you will have an accent. Responding to these new findings about the role that the environment plays in physically shaping the brain, especially during the critical periods of development, the National Institute of Mental Health has refocused its mission. Its goal now is to promote earlier and earlier intervention strategies to prevent some of the bad things that are associated with stressful environments during childhood. In its recent report, Starting Points, the influential Carnegie Corporation of New York said the first three years of a child's life are vitally important to brain development. Unfortunately, for a growing number of children the period from birth to age three has become a mental wasteland. Society, said the Carnegie report, needs to invest adequate resources in helping these children at this critical period in their lives if we are to stem the growing epidemic of violence. There is increasing concern that the lack of proper stimulation, may be damaging brains. The same may be true of too much exposure to the wrong kind of stimulation, such as violence. Indeed, in the last 25 years there has been a doubling, of the rates of crimes of violence, depression, suicide, and drug and alcohol abuse. The culprit, many scientists now fear, may well be brain cells that do not learn what they are supposed to do because they have been deprived of normal stimulation on the one hand and overexposed to violence and stressful events on the other. For millions of American children the world they encounter is relentlessly menacing and hostile. So, with astounding speed and efficiency, their brains adapt in an effort to protect them by preparing for battle. Cells rewire trillions of connections that create the chemical pathways of aggression. But the brain does not have to be victimized. It can be prevented from going down the wayward path. Craig Ramey of the University of Alabama showed that what Greenough did with animal brains by providing stimulating experiences, he could do with children. Starting as early as 6 weeks of age, his intervention program showed that impoverished children exposed to nurturing and mentally stimulating experiences could be prevented from having low IQ's and mental retardation. After 3 years children in the intervention group had IQs in the normal range, around 100, whereas children living in similar poor neighborhoods, but who were not in the intervention program, averaged IQs that were 20 points lower. By age 12, 50 percent of the children in the control group, those who continued to live unstimulating lives, had failed one or more grades. But only 13 percent of the children in the intervention group had a similar failure record. Early intervention also seems to work on middle class children. Using Ramey's stimulating learning experiences, Jeanne Brooks-Gunn of Columbia University's Teachers College wanted to find out if she could raise the IQs and reduce behavioral problems of premature infants, who come into the world at a biological disadvantage. In a study of nearly 1,000 premature infants at 10 centers, those in the intervention group had modest, but significantly higher IQs than infants in the control group after three years. Importantly, her study included middle class families as well as poor ones, a spectrum that other intervention studies had not looked at. It also included middle class blacks and poor whites. These across-the-board intellectual and behavioral improvements among all socioeconomic levels indicate that early intervention has universal powers. Did the intellectual benefits last? The gains remained solid after five years and appear to be holding now, some eight years later.Just as Wiesel and Hubel showed that brain cells that normally process vision won't work if they are not stimulated, Saul Schanberg of Duke and Tiffany Field of the University of Miami showed that touch is also critical to the brain. Newborn mice separated from their mothers stop growing. The researchers found that the mothers' licking was the cue that told the pups that all was well and that they could continue their development. Without the licking the brains of the pups went into a survival mode. The absence of licking meant that the mother was not present, so there was no food. Their brains shut down the feeding response to conserve what energy the animals had. After a prolonged absence of licking, the pups failed to thrive. But the pups' feeding response could be restored when the mother resumed licking them, or when researchers stroked them with a wet artist's brush. Knowing that premature infants who well were kept in incubators bearing "Do Not Touch" signs did not thrive, Schanberg and Field got an idea. Human babies are not licked, but they are held and their backs are rubbed. The researchers found that touching preemies in this way affected their brains, just as it did the infant mice. Stress hormones declined, and the preemies doubled their growth rate. Thanks to this discovery, preemies are routinely held and rubbed and they develop at a more normal rate. Even short-term babies can benefit from massage. Field studied normal-weight babies born to depressed adolescent mothers. These infants have two strikes against them---their stress hormones are churning and they receive little stimulation from their mothers. Field compared 15 minutes of massage twice a week to a similar period of rocking to determine which technique was more effective at calming these babies. She found that massaging significantly lowered stress hormone levels in the babies, and that they cried less, gained more weight and showed greater improvement in measures of emotionality, sociability and soothability temperament. Rocking did not do much for the babies. Once the door into the brain was opened, was only a matter of time before scientists realized they could study the biology of violence. Researchers are finding that genes can be altered by environmental stimulation to work harder or to work less, sometimes increasing a person's risk of aggression or violence. They are also finding gene mutations that are more easily affected by environmental factors, such as alcohol and stress, making some people who have these mutations even more prone to violence. As a society we seem to be inadvertently contributing to the increased rate of violence by what we do and what we fail to do. Among the factors that are now implicated as potential contributors to the genetic-environmental link to violence are the great increase in births to unmarried teenagers, babies born into overcrowded and impoverished environments, brain injuries, alcohol, cocaine, steroids, and lead poisoning. As we learn how to use the brain, we are also learning how easily it can be damaged by the lack of the right kind of stimulation or too much of the wrong kind, violence. The wonderful world of molecular biology is also revealing the brain's self-healing powers--- hormones and other chemicals that nurture and sustain brain cells. When these chemicals begin to dry up, as they sometimes do with age and with some mental disorders, brain cells wither and die. Memory loss, Alzheimer's disease, Parkinson's, Huntington's, and other degenerative diseases of the brain are now believed to be the biological desert created when these rejuvenating chemicals vanish. If we can measure when our brain-nurturing chemicals start to decline and restore them to youthful levels, we may be able to cure or prevent many of the things that go wrong with the brain. Among the exciting new findings: Hormones---estrogen, progesterone, testosterone and growth hormone---play key roles in maintaining many types of brain cells. Some of these hormones, which may become the first effective drugs to prevent Alzheimer's disease and memory loss, have already produced promising preliminary results. Estrogen, once thought to be solely a female sex hormone involved in reproduction, is turning out to be an important rejuvenator of female and male brains. A number of studies now show that women who are on estrogen replacement therapy after menopause have a dramatically lower risk of developing Alzheimer's, in addition to their greatly reduced risk of heart disease and osteoporosis. Drugs are improving learning and memory in animals and some of them are being tested in humans. In one study at Northwestern University Medical School, researchers are testing a drug that boosts memory in normal older adults by 50 percent as measured on a test. Brain chemicals called neurotrophic factors keep cells healthy and communicating with each other. When these factors diminish or disappear, the brain cells they nourish shrivel up. Prodded by the National Institutes of Health, scientists are gearing up to test one of them, nerve growth factor, to determine if it can stop the destruction caused by Alzheimer' s disease. Other neurotrophic factors may make it possible to grow new brain cells to replace missing ones. Is there a bottom line to this new research? Most certainly. The amazing discovery of the brain's plasticity---its ability to physically rewire itself to become smarter---makes mental stimulation, in the long run, more essential to the body than food. That the brain thrives with good nourishment is a concept that has profound significance for individual achievement and for the way parents raise their children. The brain's food is education. Just as the food we eat gives our immune systems the strength to fight off life-threatening infectious germs, education protects us against bad choices. In effect, education acts like a vaccine that boosts our mental powers, making us more resistant to illness and premature aging. Education provides such strong immunity, in fact, that people who acquire more of it are living longer than ever before while those who don't have it are falling farther behind. It is the secret to a healthier, longer life. For people who don't grab at the opportunity for education, the news is grim. They are on the wrong end of a widening gap between people who build more brain power and those who ignore it, and they are more likely to die younger. Despite an overall decline in death rates in the U.S. since 1960, poorly educated low income white males die at rates that are three to seven times higher than white men with better education or higher income, Dr. Gregory Pappas of the National Center for Health Statistics found in a 1993 study. The earlier education is acquired, the more impact it has against sickness and early death. Education throughout life acts like a continuing series of booster shots. Education works in two fundamental ways: Biologically, by laying down significantly more connections between brain cells that accompany learning. Memory, as a result, is increased and the additional connections also provide a buffer against the destructive forces of Alzheimer's disease. Behaviorally, by promoting positive values and attitudes about health, higher self-esteem, effective coping skills, access to preventive health services and association with people who have similar views. At the same time, education reduces risky behaviors such as smoking. the long run, more essential to the body Just as some people fail to get vaccinated against common childhood infections, others fail to take advantage of the immunizing effects of education. Half of all high school students in Chicago and some other large cities, for instance, fail to graduate. The toll this takes on the brain is staggering. Children born to mothers who have less than 12 years of education have a fourfold increased risk of mental retardation, said Dr. Marshalyn Yeargin-Allsop, a medical epidemiologist at the CDC's Division of Birth Defects and Developmental Disabilities. "This regardless of race," she said. "White children had the same fourfold risk as black children if their mothers didn't complete high school." A CDC study of more than 1,000 children showed that mild retardation, defined as having an IQ between 5O and 70, occurs at the rate of nearly one in 100 children. The biggest risk factor for mild retardation is the mother's low educational level, which far exceeds the risk posed by poverty. About 22 percent of all births in this country are to mothers with less than a high school education, Yeargin-Allsop said. These women often do not know how to provide stimulation---such as talk, toys, and physical activity---to their infants, which can lead to stunting of the brain during the crucial first three years of life, she explained. Mild mental retardation is generally believed to be caused by a failure to provide the brain with the kinds of experiences from its surrounding world that it needs to develop to its maximum capacity. Early educational intervention programs for children at-risk have shown that they can increase IQ levels by 15 points or more. "At least half of the cases of mild mental retardation are preventable," Yeargin-Allsop said. "We can leapfrog over the risks if young people stay in school and get as much education as they can." If early education is like a vaccine against risk factors, then giving it to poor, deprived children should help protect them as they grow older. That's what David Weikart, president of the groundbreaking High-Scope Perry Preschool Study in Ypsilanti, Mich., set out to prove in the late 60s. Weikart randomly divided 127 African American children ages 3 and 4 into two groups. The children were born in poverty and had a high risk of failing in school. One group received intensive preschool education 2.5 hours a day for 3.0 weeks. The other group served as controls. "The educational program focused on getting kids to make choices between things that might either be good or bad for them and to invent solutions to the problems they were working on," he said. Now, 27 years later, the children who were in the intervention program are doing significantly better as adults than the controls. Seventy-one percent of them finished high school compared to 54 percent of the controls. And they have less risky lifestyles. The children who were in the education program have less than one-third the risk of being arrested for drugs as the controls, and girls in the program are one-third less likely to have babies out-of-wedlock than their peers in the control group. Those in the program are less likely to have been on welfare and more likely to own their own homes, have good jobs and be in a stable marriage.