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Enzyme May Help Brain Clean the Slates Healthy News A molecular "eraser'' has been found in the brain, scientists report Thursday, suggesting that without it our memory tracks would function about as well as a computer without a delete key. Reporting in the journal Nature, scientists describe the intricate workings of an enzyme of forgetting called PP1, shorthand for protein phosphatase 1. And if you find that name hardly worth recording and soon forget it, it might be because you have a healthy amount of the stuff. A series of experiments on genetically altered laboratory mice suggests that the newfound mental eraser is part of a healthy tension between learning and unlearning that keeps synaptic circuits from becoming saturated early in life with needless information. The same memory constraint, perhaps running in overdrive, may play a role in some forms of age-related memory decline, suggesting a potential target for memory-enhancing therapies if further studies can determine just how PP1 might figure into memory-related syndromes suffered by humans. Alcino Silva, a neuroscience professor at UCLA who co-wrote a commentary on today's study that also appears in Nature, said the experiments moved the scientific understanding of learning a critical step forward, although much of the mystery remains. "A great deal is known about the molecules of learning and memory,'' he said, "but this is the first piece of evidence I know of about the mechanisms of forgetting.'' Conditions such as Alzheimer's disease, strokes and traumatic brain injuries also can wipe out memories, but that occurs typically through the death of millions of brain cells. The neurochemical system described in today's study is much different and far more subtle. Although chronic forgetfulness can be a symptom of disease, today's study suggests it also can be an ordinary part of healthy mental functioning. One thing the study makes clear, Silva said, is that "forgetting is not just chaos. It's an organized process.'' Conclusions are tentative because no human experiments have been done. In fact, it's difficult even to conceive of any practical way to test how the activity of particular brain chemicals might explain what goes in our heads when we, say, memorize a new home phone number and forget our old one. But scientists said there is every reason to suspect that rodent neurobiology is not all that different from our own. "There are active processes to get rid of information,'' said Isabelle Mansuy, a neurobiologist at the Swiss Federal Institute of Technology in Zurich and senior author of today's study. The findings underscore one of the most fundamental insights arising from a recent flood of brain research: Healthy mental function, like that of virtually all body systems, is a matter of keeping opposing forces in a state of healthy tension, a condition known as hemeostasis. In this case, the brain seems to be genetically hardwired to perform a complex balancing act between recording information and wiping the slates clean. Although it might seem preferable to minimize the latter business, an inability to forget trivial matters can be a serious disability - as popularized in the 1988 hit film "Rain Man,'' in which Dustin Hoffman depicted an individual dealing with autism and savant syndrome. Dr. Darold Treffert, a Wisconsin physician who served as a consultant on the film, said he always suspected that some savants with seeming total recall "may not have so much a fantastic ability to remember, but an inability to forget.'' Whether PP1 deficiencies might help explain the problem remains to be seen. But scientists said there is little doubt that a healthy brain needs the ability to perceive what is worth remembering and forget the rest. "There needs to be a balance in the brain between positive processes and negative processes,'' Mansuy said. "It's like any natural function. Forgetting is part of the homeostasis of the brain.'' In the new experiments, Mansuy and her colleagues set out to find the molecular underpinnings behind the fact that memories usually lose fidelity and eventually vanish with time. Another question they sought to answer is why "cramming'' is not a terribly effective way to learn, as compared with dividing study sessions into short periods with breaks in between. Earlier evidence had suggested that a gene encoding the PP1 enzyme was involved, acting in combination with some other key molecules. So researchers bred a line of mice that produced a neurochemical inhibitor of PP1, effectively blocking the action of the enzyme. The PP1-inhibited mice and normal control animals were then put through a series of learning tests - finding their way through cloudy water to a submerged platform, for instance - to determine how the active molecule functioned. Results showed that PP1 "determines the efficacy of learning and memory by limiting acquisition and favoring memory decline,'' the scientists found. Inhibiting PP1 tended to prolong memory after learning, and the genetically modified mice proved to retain information long into their old age, while normal aged mice soon forgot what they had been taught. The findings "emphasize the physiological importance of PP1 as a suppressor of learning and memory, and as a potential mediator of cognitive decline during aging,'' the scientists concluded. Brain Cell "Chorus" Appears As Attention Increases Johns Hopkins University The sudden emergence of a brain cell "chorus" from the cacophony of normal brain cell activity may enable the brain to pay close attention to one item in a flood of incoming sensory information, according to a report in Nature. The report, based on data acquired from monkeys, suggests that a baseball player tracking a fly ball through a cloud-cluttered sky, a driver reaching into a pocket to feel for keys, and a high-school student seeking a cafeteria dish that smells edible could all have something in common: Some of the nerve cells in the cortex, the sophisticated outer layer of the brain, may be sending messages in unison to allow them to pay attention to a single stream of sensory input. "Every second, we get millions or hundreds of millions of bits of information coming in from our senses," says Ernst Niebur, assistant professor of neuroscience at the Krieger Mind-Brain Institute at The Johns Hopkins University. "And we have to decide, every second, which part of it is important and which part is not important." "The nerve cells which represent the important information need a way to stand out from the crowd of other information," says Peter Steinmetz, lead author on the paper and a former postdoctoral scholar at the institute. "Firing synchronously – like singers in a chorus -- is one way to stand out from the crowd." Scientists produced the new finding by re-analyzing data gathered over several years. Institute scientists Ken Johnson, and Steve Hsiao had been monitoring brain cell activity in monkeys who were performing simple tasks that required them to focus their attention on visual or tactile stimuli. Tasks included identifying which of three white squares of light on a video monitor was beginning to dim, and comparing the shape of raised letters or figures pressed against a finger. Applying a technique perfected by Hopkins neuroscientist Vernon Mountcastle, researchers used seven electrodes to simultaneously monitor individual brain cell activity in the monkeys as they worked. They originally analyzed the data they gathered for changes in the firing rate of brain cells as the animals switched attention between tasks. When Niebur arrived at Hopkins a few years ago, researchers started talking about taking another look at the data. Niebur and other theoretical neuroscientists were speculating that the brain might encode information both in the firing of individual brain cells and in the timing of those firings. "It's been shown in animals that the firing rate of neurons can go up by a factor of 2 or 3 when they start to pay attention to a stimulus," Niebur says. "But it seems to run the risk of confusing signals if you try to code for two different things -- the stimulus itself and the degree that one should pay attention to it -- with one type of signal, the rate at which neurons are firing." Niebur says the two different signals have to be connected. What your senses perceive will influence how much attention you pay to them, but, he said, "it seems like a good idea if you can have two different but related signals that you can use to represent these two things." An increase in the number of nerve cells firing in unison could represent just such an independent, but related, second signal. Hsiao and Johnson had data from three earlier experiments appropriate for testing the theory. Steinmetz, now a post-doctoral scholar at Caltech, combined currently available computer power with a cutting-edge statistical technique to determine if nerve cells were firing synchronously and if the strength of that synchrony changed when the monkeys needed to pay attention. "Detecting synchronous firing reliably has been difficult in the past because of the large amounts of data that need to be analyzed, but one outcome of the computer revolution has been the ability to perform this type of testing in reasonable timeframes," Steinmetz says. The results of the analysis, according to Niebur, suggested that when the monkeys were paying close attention to the stimuli, "the amount of synchronous firing appeared to increase in a sizable fraction of the neurons involved in these tasks." Such a mechanism could have intriguing connections to basic nerve cell structure and function, Hsiao notes. Nerve cells frequently receive incoming signals from not just one but several different branch-like structures known as dendrites. Unless the signal is very strong, receiving a signal on any one dendrite doesn't necessarily guarantee that the nerve cell will pass on the message. "If all the neurons upstream are firing synchronously, though, that strongly increases the possibility that the nerve cell will pass the message on downstream," says Hsiao, an associate professor of neuroscience. "We were lucky that these three groups could come together for this team effort," Hsiao comments. "The Mind-Brain Institute is one of a very few places in the U.S. where you could see such a unique and close collaboration between experimental, theoretical, and computational neuroscientists." All 3 research groups plan to follow up on the finding in the future. "I'd like to go back to an earlier stage in this process, and look for some type of oscillatory signal that we're thinking could proceed these synchronized nerve cell firings," Johnson, a professor of neuroscience, says. Niebur and Hsiao expressed interest in finding out what happens to synchrony rates if the test subjects fail to successfully complete the task they're concentrating on. Steinmetz's current research includes an investigation how strongly the neurons need to synchronize their firing to be "heard." Funding for this study came from the National Institutes of Health, the Alfred P. Sloan Foundation and the National Science Foundation. Other authors were Arup Roy and Paul Fitzgerald, graduate students in neuroscience at Krieger Mind-Brain.

Fingerstick Test for Celiac Disease Healthy News A new test for celiac disease (CD) will be particularly useful to the sufferers of classical celiac disease who are unaware of their condition because they do not have the signs and symptoms typically associated with CD. They have a risk of developing full-blown CD later in life, along with such complications as bowel cancer, infertility, and autoimmune diseases. The new test, an enzyme-linked immunosorbent assay (ELISA), does not require a blood draw. Using a specimen collection kit, medical professionals and patients alike can simply prick the end of a finger to collect a tiny sample of blood for use in the test. An analysis known as an IgA tissue transglutaminase (tTG) autoantibody assay is then performed, and results are available within 10 days. A detected increase in the antibody levels indicates the probability of celiac disease. The test was developed by York Nutritional Laboratories (Hollywood, FL, USA). "This entire noninvasive process is far less expensive and much more convenient than the intestinal biopsy procedure used in the past," said Martha Gonzalez, operations manager of York. Researchers Grow Brain Cells at SDSU Healthy News South Dakota State University has long had a reputation for involving students in crop research. But what is being grown in a small room on the top floor of the pharmacy building at State goes beyond traditional row crops or even exotic plants. Three undergraduate students are working with two assistant professors in the College of Pharmacy to grow human brain cells. It is one of a handful of places in the world where the work is being done, according to the husband-wife research team of Suman Mukherjee and Manisha Sonee. Although both work with and help to grow the cells, their research falls into separate areas. Mukherjee experiments with a compound that could be used in the prevention and treatment of Alzheimer's and Parkinson's diseases, which affect the brain. Sonee seeks to better understand the mechanical functions of cells when they are exposed to Alzheimer's Disease conditions. Stacy Peters of Pipestone, Minn., says each of the students work on both projects. Peters, who started work late last summer, says she was intrigued by the topic. "The fact that they were human brain cells and the work is concentrated on treating and preventing neurological diseases caught my attention." Fellow students Carisa Finke of Pipestone and Stephanie Villmow of Delmont, S.D., got a head start on Peters in their work. Finke started in January 2001; Villnow started last May. As a result of a proposal that each student wrote on their role in the project, they were selected for scholarships that entitled them to work with the researchers. "I love it. It's fun," Finke says of the project. "I really wanted to get this project because I've always been interested in Alzheimer's Disease and that's what my project primarily involves." Villmow reports that "Carisa had started working already" with Mukherjee and Sonee. "She was telling me the neat things she was doing, and I didn't have plans for the summer. I thought I should do research. It's probably a once-in-a-lifetime possibility." Mukherjee says the students, who are in their fourth year of the six-year PharmD program, are an integral part of the project. "We have to spend quite a bit of time with them to do the techniques correctly," he says, "but once we do, we rely on them to do it all." He describes the students as "first rate. They don't look at it like a job. They look at it like a challenge, and that takes it to a higher level. I have been amazed by their grasping of these different concepts, how they do the experiments, their hard work, and general enthusiasm. "None of my students have had prior research experience. They start out in the summer with varying degrees of apprehension, but by the end of the summer, they're usually working Saturdays and Sundays." The research is not required for the students to receive their degrees. But Finke and Peters are both considering careers in pharmaceutical research and know their work with Mukherjee and Sonee could help them solidify their post-graduation plans. Finke first experienced undergraduate research in summer 2000, when she collected data on cheese and milk for David Henning, an associate professor in dairy science. Villmow says that learning the techniques needed to grow brain cells isn't easy. "There is a lot of practicing your technique with water." After about a month, she was prepared to feed the brain cells. But after ten weeks on the job, she wasn't prepared to do the volatile task of dividing the cell cultures. It took about six months for Mukherjee and Sonee to "get a handle on" how to grow human cortical neurons, the cells found in the front part of the brain where a portion of the memory function occurs, Mukherjee said. "Human brain cells are very difficult to grow. By nature, they're resistant to duplicating. We have to feed them and coax them into dividing," says Mukherjee, who started working with the cells shortly after he joined the SDSU faculty in fall 1999. "Brain tumor cells are easier to grow, but Alzheimer patients most likely do not have brain tumors," he says. The researchers, who also have a teaching load, find their schedules "completely dictated by the cells," says Mukherjee, who, like his wife, holds a bachelor's degree from Jadavpur University in Calcutta, India, and a doctorate from the University of Southern California. Sonee notes that the cells "need to be fed every day, and when you're working with them, you have to be very gentle with them. You have to maintain them in certain conditions" -- just the right temperature, humidity, and carbon dioxide level. "And they have to be at the right concentration. There can't be too many or too little," she adds. The cells are fed a commercially-made liquid nutrient mix. Although an experienced scientist can feed the cells in an hour, providing a serving of "brain food" to the cultures is a bit more complicated than squirting an eyedropper of the red fluid into a fish tank. Sterile conditions are the key. The room, formerly a prep area for a student lab, is equipped with $61,000 worth of instruments for cellular research. A key component is the biological safety cabinet, which has an ultraviolet light to kill microbes that would feast on the cells. To further eliminate microbes, the cabinet and all instruments are wiped down with a seventy percent ethanol solution. Operators must wear gloves and be careful not to let their hands pass over the small plastic flasks where the cells are being grown. Until the researchers are ready to start growing the cells, the vials of commercially purchased cells are kept in liquid nitrogen. After research on a particular batch of cells is completed, the sample is refrigerated at --eighty degrees to keep enzymes from making further changes to the cells. The preservation technique allows for later research on cells, Mukherjee said. Before the cells are fed, the nutrient is heated to thirty-seven degrees centigrade, which is body temperature, he said. The work is exacting. "We just can't afford to have these cells die on us because if these cells die, you can easily lose a couple months of work in two minutes," Mukherjee said. So far, the couple has had only one major cell die-off, he said. Growing the cells is a science in itself, but that only starts the work of Mukherjee and Sonee. He uses the cells to better understand why cells die, as they do in Alzheimer's and Parkinson's diseases, and what can be done to combat that. Mukherjee has found that a compound using nicotinamide, a vitamin which he purchases, is effective in preventing cell death. Nicotinamide converts to ATP (adenosine triphosphate), which provides the cell its energy, he said. "Our brain is separated from the rest of the body by a barrier. It prevents poisons from getting into the brain. Most of the drugs we take cannot get into the brain, but nicotinamide is a compound that can get into the brain," Mukherjee explains. Sonee's work examines both healthy brain cells and those damaged by conditions that mimic Alzheimer's Disease. By gaining a greater understanding of how motor proteins work and how the transportation system within a cell functions, she hopes to give researchers a platform from which they can better seek a cure or find a cause for Alzheimer's Disease, she said. Eventually, they hope to gain funding from the National Institute of Health or other national organizations for their work. In the meantime, the College of Pharmacy's research "farmers" diligently grow the cells that are needed to help solve two of the world's most tragic diseases.

Autism:Theory of Mind Written by Stephen M. Edelson, Ph.D. Center for the Study of Autism, Salem, Oregon A relatively new hypothesis in the field of autism has been labeled 'Theory of Mind.' This idea has received much attention including a recent book in 1995 by Dr. Simon Baron-Cohen (Mindblindness, Cambridge, Mass.: The MIT Press) and an article by Dr. Uta Frith in Scientific American in 1993. Theory of mind refers to the notion that many autistic individuals do not understand that other people have their own plans, thoughts, and points of view. Furthermore, it appears that they have difficulty understanding other people's beliefs, attitudes, and emotions. Many of the tasks used to test this theory have been given to non-autistic children as well as children with mental retardation, and the theory of mind phenomenon appears to be unique to those with autism. In addition, theory of mind appears to be independent of intelligence even though people with Asperger's syndrome exhibit this problem to a lesser degree. Interestingly, people with autism have difficulty comprehending when others don't know something. It is quite common, especially for those with savant abilities, to become upset when asking a question of a person to which the person does not know the answer. By not understanding that other people think differently than themselves, many autistic individuals may have problems relating socially and communicating to other people. That is, they may not be able to anticipate what others will say or do in various situations. In addition, they may have difficulty understanding that their peers or classmates even have thoughts and emotions, and may thus appear to be self-centered, eccentric, or uncaring. Although this is an egocentric view of the world, there is nothing in the theory of mind to imply that autistic individuals feel superior to others. The vital question which must be asked is: How does one teach individuals with autism to understand and acknowledge the thoughts and feelings of others? One of the methods used to teach autistic children and adults this concept is an intervention developed by Carol Gray called 'social stories.' These short stories describe different scenarios which allow autistic individuals to understand themselves and others better. These stories may motivate them to start asking questions about other people and at least recognize that different individuals think in unique ways. An information packet can be purchased from Carol Gray for $5.00. Her address is: Consultant to Students with Autism, Jenison Public Schools, 8375 20th Avenue, Jenison, MI 49428. Autism and the "Theory of Mind" Debate Robert M. Gordon and John A. Barker Recent research has established that by the age of 4 most developmentally normal children understand that people sometimes respond to the world not as it actually is but merely as they believe it to be. With this understanding, children are better able to anticipate the behavior of others and to attune their own behavior accordingly. In mentally retarded children with Down's syndrome, attainment of such competence is delayed, but it is generally acquired by the time they reach the mental age of 4, as measured by tests of nonverbal intelligence. Thus from a developmental perspective, attainment of the mental age of 4 appears to be of profound significance for acquisition of what we shall call psychological competence: possession of the skills and resources people routinely call on in the anticipation, explanation, and social coordination of behavior. There is one notable exception, however. Most autistic children lack much of this competence even at significantly higher mental ages, according to a number of recent experimental studies. Most do not seem to understand that people's actions and emotions are contingent on their beliefs. Rather than treating other people as subjects with "points of view," they frequently give the impression of "treating people and objects alike." Asked what the brain does, autistic children speak of it as making people move or run, whereas most children first mention thinking or feeling. Philosophers have sometimes found it useful to invent imaginary people who treat their fellows as, literally, mindless beings. The exotic creatures of philosophical fiction appear congenial and well-adjusted, however, in comparison to those real people who are severely handicapped by autism. People with autism, even many of the most intelligent among them, apparently never succeed in developing a normal understanding of many of the psychological dimensions of human existence, and as a result, they fail to achieve normal interactions with other human beings. Many autistic people are also abnormal in respects other than psychological competence. The majority are mentally retarded. But their striking failure in many psychological tasks does not appear to be accountable in terms of any broad deficit in intellect. It has therefore been argued by a group of leading researchers that autism is characterized by a specific deficit in psychological competence, or what they call possession and use of a "theory of mind" (Baron-Cohen, Leslie, & Frith 1985; Leslie 1987; Frith 1989; Baron-Cohen 1990). Some Pivotal Experimental Results According to many accounts, the major watershed in the development of psychological competence is the capacity to deploy the notion of belief, and in particular the capacity to attribute beliefs that are false or contrary to fact. A classic experimental study, Wimmer & Perner 1983, focuses on false belief and establishes that in normal children this capacity becomes apparent at approximately the age of 4. In the original experiment, children are presented a story, illustrated with puppets, in which the protagonist places an object in one location and subsequently, while he is out of the room and without his knowledge, someone else relocates the object. Where does Maxi go to retrieve his candy when he returns to the room? We of course would predict that he will look for it in the wrong place, and so do most children of age 4 or older. Children under about the age of 4, however, point to or otherwise indicate the actual present location of the candy. Evidently they are unable to adjust for the fact that the protagonist was not in a position to know that the object was relocated. They treat all the facts presented to them in a story as accessible to the protagonist, as if nothing were beyond his ken. It doesn't matter whether something happens in plain sight of the protagonist or whether he is epistemically handicapped. The experiment has been replicated a number of times and it has held up very well and been supported by other research. Even more striking than the results of the original experiment were those reported in Baron-Cohen, Leslie, & Frith 1985. In this study, a test similar to the one used in Wimmer & Perner 1983 was applied to a group of clinically normal 4-year-old and 5-year-old children, a group of mentally retarded children with Down's syndrome (mean chronological age = 10, mean nonverbal mental age = 5) and a group of high-functioning children with autism (mean chronological age = 11, mean nonverbal mental age = 9). It was found, on the one hand, that the mentally-retarded Down's syndrome subjects gave the "right" response about as frequently as the normal children did. On the other hand, most of the high-functioning autistic subjects gave the wrong response. Even those who had attained the mental age of 9 typically performed at the 3-year-old level on false-belief tasks. Despite being "smarter" than the other subjects, the autistic children appeared to suffer from a specific deficit in at least this aspect of psychological competence. Results consistent for the most part with those reported in Baron-Cohen, Leslie, & Frith 1985 have been obtained in a variety of subsequent studies.[3] In addition, a later study by Baron-Cohen, Leslie, & Frith (1986) employed a largely non-verbal test in which children were asked to put the frames of a picture story into the proper sequence. Where the sequence was one of mechanistic causality, children with autism performed at least as well as normal children and those with Down's syndrome. But where the "right" sequence (recognized immediately by normal adults) depicts a story involving false belief, the performance of autistic children was no better than chance, and far worse than that of normal and Down's syndrome subjects. Is Psychological Competence Based on a Theory? We shall assume in this paper that the available evidence largely favors the hypothesis of a specific deficit in psychological competence. Whether we should characterize it as a "theory of mind" deficit, following Baron-Cohen, Leslie, and Frith, depends on whether we wish to accept the implicit assumption that psychological competence consists in the possession and use of a theory. This is indeed a popular assumption. For the past quarter-century a dominant view in philosophy and the cognitive sciences has been that the resources that underlie common-sense explanations and predictions of behavior chiefly consist in a tacit body of propositional knowledge roughly comparable to a scientific theory. The alleged theory posits unobservable mental states such as beliefs, desires, intentions, and feelings, linked to each other and to observable behaviors by "law-like" principles. These principles are applied to observable situations by way of logical inferences that generate predictions and explanations of behavior. The theory is supposedly called upon by people of all cultures and virtually all levels of intelligence to explain and predict the behavior of others. To apply the theory, it is said, one neither needs nor typically possesses any conscious awareness of the principles one is applying. Careful reflection, however, can often bring them to light. And once they are provided with verbal garb, the principles typically seem obvious, commonplace, and platitudinous--which is taken to be good evidence that they constitute unquestioned presuppositions of a tacit folk theory. The view that common-sense explanations and predictions of behavior are theory-based is called the "theory" theory. Despite general acknowledgement that this view has serious deficiencies, it was until recently widely conceded that it had no plausible alternative: it was, as Jerry Fodor put it, "the only game in town." Indeed, it has been presupposed in most debates in the philosophy of mind, particularly the debate between those such as Fodor, who think our tacit common-sense theory likely to be vindicated in large part by future science and those (the "eliminativists") who believe future science will show it to be radically mistaken and misconceived. According to some developmental psychologists who accept the theory-theory, children acquire psychological competence by a process of theory-construction and theory-change, replacing inadequate laws or principles with better ones, progressing toward mature conceptions of mental states such as belief and desire. Consider how on this view one might explain the difference between the way a 3-year-old and a 4-year-old answers the question, "Where will Maxi go to get his candy?" A 3-year-old might reason (consciously or unconsciously) as follows: To get x, people will go to wherever x is. And Maxi's candy is in location B. Therefore, to get his candy, Maxi will go to location B. (The same conclusion could also be reached using an immature notion of belief shaped by the principle, "If it is the case that p, then people believe that p.") In contrast, a typical 4-year-old could deploy the notion of a belief that may or may not correspond to fact. The child might reason, consciously or unconsciously, along the following lines: Principle: People who put an object in location l will typically believe just afterward that it is currently in location l. So, just after Maxi put his candy in location A, he believed that his candy was currently in location A. Principle: People who believe that something is currently in location l will typically continue to believe that it is in location l, unless they come to believe it (was) moved. Principle: Typically people come to believe that x (was) moved only if they saw x move (being moved) or are told that x (was) moved. But Maxi neither saw his candy being moved nor was told that it was moved. So, when Maxi returned, he believed that his candy was currently in location A. Principle: To get x, people will go to wherever they believe x is. Therefore, to get his candy, Maxi will go to location A. The assumption that psychological competence consists in the possession and use of a theory is shared by many recent investigators of the development of psychological competence: the field of investigation has even come to be called, "the child's theory of mind." Developmental psychologists inherited the term "theory of mind" from an article that asked whether the chimpanzee has a theory of mind (Premack & Woodruff 1978). The authors of that paper used the term very loosely, however. They gloss the term as follows: In saying that an individual has a theory of mind, we mean that the individual imputes mental states to himself and others. (p. 515) This suggests that Premack and Woodruff were introducing the term "theory of mind" merely as an abbreviation of "capacity to attribute mental states." If that were their sole intent, then of course they would be leaving open the question, "What is the basis of the capacity to attribute mental states?" But their choice of the term theory suggests that they were not leaving this question open but rather taking for granted a certain answer to the question. They were accepting the conjecture that it is possession and use of a theory that gives individuals (human beings and possibly chimpanzees) the capacity to attribute mental states. Indeed, they did attempt to justify their use of the term theory on the grounds that mental states are not observable and that people are able to make predictions on the basis of these attributions. And at the time they were writing there seemed to be no plausible alternative way of explaining how people might make predictions on the basis of attributions of states that lie "behind" behavior. Some of the developmental psychologists who borrowed the term "theory of mind" from Premack and Woodruff also slide too easily from "capacity to attribute mental states" to "theory of mind" (as noted in de Gelder 1993). They vacillate between the innocuous assertion that by age 4 children are able to attribute mental states and the extravagant speculation that by age 4 children have a relatively mature theory on the basis of which they are able to attribute mental states. Considerable care should be given, therefore, to interpreting Baron-Cohen's claim that people with autism have a "theory of mind" deficit. If he is to be taken as saying only that normal children and those with Down's syndrome have a capacity to make a type of attribution that autistic children do not make, then he is putting forward a very interesting claim that does appear to be warranted by the experimental results he cites. But if he is to be taken as saying that normal children and those with Down's syndrome possess and use a theory (or part of a theory) which autistic children alone do not possess and use, then he is making a claim that appears to be called into question by some of the experimental results he cites in its support. For children afflicted with Down's syndrome, who evidently have the psychological competence characteristic of their mental age, are notably deficient in theoretical abilities; whereas children afflicted with autism, who appear to be psychologically incompetent, are not generally deficient in theoretical abilities (again adjusting for mental age). Why would autistic children who in some cases do even better than the average normal child in mastering theories of other sorts fare so badly in this particular domain? And, even more counter-intuitive, how can it be that Down's children with IQ's as low as 50 are able to master this "theory" about as well as normals do (albeit a few years later), when they master no other theory? In short, one drawback of the theory-theory is that it is not easily squared with the findings regarding the psychological competence of children with Down's syndrome and the psychological incompetence of relatively intelligent children with autism. We think the evidence suggests that the psychological competence that normal children develop but autistic children do not develop is based not on a theory but rather on a skill that does not essentially require the aptitudes tested in typical "IQ" tests. That is why retarded children with Down's syndrome, even those who in large degree lack these further aptitudes, prove to be psychologically competent. (Of course, one may reasonably expect the relevant skill to be refined and enhanced by these further "IQ" aptitudes. Hence it is not a consequence of our view that low-IQ Down's syndrome children are as likely as normal children to become successful novelists, playwrights, or psychologists.) Although clearly not deficient in theoretical powers relative to their mental age, autistic children are in other respects very markedly different from other children of the same mental age, including those with Down's syndrome. Some of these differences can reasonably be attributed in large part to their impaired psychological competence. For example, autistic people are notoriously odd and limited in their capacity to communicate with others, both verbally and nonverbally. They also have a severely diminished capacity to enter into normal social relationships, especially with peers. Although these handicaps no doubt set them further behind the pack in psychological competence, the more important causal relationship seems to be the converse: without a level of psychological competence beyond that attained by most autistic people, normal communication and normal social relationships are altogether impossible (Baron-Cohen 1988; also Frith 1989). Thus whatever may prove to be the key to the psychological incompetence of autistic individuals will probably also be the key to their social and communicative impairments. Pretending and Simulating There are, however, other autistic abnormalities that cannot be attributed chiefly to psychological incompetence. Among these is the often-remarked failure of autistic children to engage in spontaneous pretend play, whether in conjunction with others or alone. Normal children and Down's syndrome children spontaneously initiate pretend-play and develop the ability to participate in complex, interactive forms of it before they develop the psychological competence required in false belief tasks. In stark contrast, the behavior of children with autism characteristically remains almost totally devoid of any signs of spontaneous pretend-play. The impoverishment of pretend play, particularly the absence of role play and mime play with imaginary objects, is well known. Although studies have shown that many autistic children can, with appropriate prompting, engage in some forms of pretend play (Lewis & Boucher 1988; Ungerer & Sigman 1981), the play is characterized by lack of spontaneity and by stereotypical, inflexible, and repetitive patterns. What is most conspicuous is the absence of other-regarding pretending, typified by role play and joint pretend play, in which two or more children act on a shared pretense (Harris, forthcoming). Might a faulty capacity for pretense, especially for other-regarding pretense, severely degrade a person's capacity to ascribe mental states? It would, according to the theory of psychological competence that we favor, the mental simulation theory. This theory asserts that psychological competence fundamentally depends on the capacity to use one's own cognitive and motivational resources to "simulate" other people, a capacity that calls on no special theory of mental states.[5] For example, we often predict what another will decide to do by making a decision ourselves--a "pretend" decision, of course, made only in imagination--after making adjustments for relevant differences in situation and past behavior. According to our version of the simulation theory, such vicarious decision-making also underlies the capacity to explain the behavior of others in terms of mental states, and probably also the very capacity to grasp the concepts of such states as belief and desire. If pretending is the key to making and understanding mental state ascriptions, then of course a developmental pathology such as autism that severely restricts the capacity to pretend should also severely restrict a child's capacity to make and understand such ascriptions, even if in other respects the child's intelligence is normal. To help the reader understand how mental simulation can yield predictions and explanations of behavior, it will be instructive to examine the logical structure of pretend play. Children enter informal games of make-believe by initially pretending something to be true that they do not believe to be true3&Mac218;4for example, that certain globs of mud are pies. By combining the initially stipulated premise with their existing store of beliefs and calling upon their reasoning capacity, they are able to obtain answers to questions not addressed in the initial premise. In the mudpie example, they would typically be able to answer the question, "How many pies are there?" And where there is more than one player, their answers would typically agree: barring a stipulation to the contrary, the answer is the same as the number of (approximately pie-shaped) mud-globs. "Which pie is biggest?" The biggest mud-glob, of course, unless otherwise stipulated. This productive feature of many games of make-believe, pointed out by Kendall Walton, closely parallels our understanding of subjunctive conditionals, as Gareth Evans suggested.[6] Wondering if the bridge would have collapsed had there not been a heavy snowfall, we pretend there hadn't been a heavy snowfall, and then ask whether, in the world thus modified in our imagination, the bridge collapsed. This, with some amendments, is the so-called Ramsey test for evaluating subjunctive conditionals.[7] But there is a further productive feature of games of make-believe. What the child does with the mudpies depends not only on the stipulated pretend-facts along with his existing perceptions and beliefs, but also his existing desires, values, and norms. Together, these fix or at least constrain the child's answer to the question: What shall I do with these pies?" This further productive feature of games of make-believe parallels our typical understanding of conditionals concerning our own actions under hypothetical or counterfactual conditions. Gordon (1986) makes the connection with pretense explicit in describing how one might predict what actions one would take upon hearing footsteps coming from the basement: To simulate the appropriate practical reasoning I can engage in a kind of pretend-play: pretend that the indicated conditions actually obtain, with all other conditions remaining (so far as is logically possible and physically probable) as they presently stand; then--continuing the make-believe--try to "make up my mind" what to do given these (modified) conditions. I imagine, for instance, a lone modification of the actual world: the sound of footsteps from the basement. Then I ask, in effect, "What shall I do now?" And I answer with a declaration of immediate intention, "I shall now...." This too is only feigned. But it is not feigned on a tabula rasa, as if at random: rather, the declaration of immediate intention appears to be formed in the way a decision is formed, constrained by the (pretended) "fact" that there is the sound of footsteps from the basement, the (unpretended) fact that such a sound would now be unlikely if there weren't an intruder in the basement, the (unpretended) awfulness of there being an intruder in the basement, and so forth. As in pretend play, an initial premise--here, the hypothetical condition--is added to one's store of beliefs, desires, and other inputs to intention-formation and decision-making. In one important respect, however, this kind of simulation is unlike children's games of make-believe (and also unlike rehearsals and drills). Although the simulation may be accompanied by autonomic arousal and some expression of emotion, it stops short of overt action. One does not carry out the decision, say, to call the police, even in overt pretend-play. Our motivational, emotional, and decision-making systems are running "off-line," as it were, disengaged from their natural output systems. The simulation theory says that in predicting, explaining and interpreting another's behavior, likewise, we run the explanation or prediction through our own motivational and emotional systems, utilizing our own capacity for practical reasoning and decision-making. In simulating another, however, it is often not sufficient to imagine being in the other's situation--that is, to employ our imagination merely to ask, "What would I do, believe, want, and feel were I in Smith's situation?" For this would leave open the further question, "What about Smith: what does Smith do, believe, want, or feel in that situation?" Rather than simulate ourselves in Smith's situation, we must simulate Smith in Smith's situation (as it appears to Smith). This would entail a further, more complex use of pretense. When one is predicting one's own actions or reactions in hypothetical conditions, the initial premise--for example, that there is a sound of footsteps coming from the basement--is simply stipulated. But when we explain or predict another's behavior in such a situation, one may in addition have to make adjustments of various kinds. These might be based on knowledge of the other's actual behavior in related situations in the past: one tries to become in imagination a person who might have acted as the other did in such situations. In false belief tasks like those presented in Wimmer and Perner 1983 and Baron-Cohen, Leslie, & Frith 1985, the needed adjustment is a simple one: just ignore one or more of the facts, and then carry on as before. In the Maxi example, what would need to be ignored is what happened while Maxi was outside, namely that his candy was moved. In effect, one follows Maxi as he goes outside, and thus fails to "see" what subsequently transpires inside: looking back, one sees only the outside of the house. Then, within the context of this pretense, one simply states where the candy is. One will then predict correctly that he will look for his candy, not where it actually is, but where it was before it was moved. Notice that, instead of invoking a special folk-psychological principle that people typically assume that objects (to put it crudely) tend to stay put, one simply relies on one's own assumption that objects tend to stay put. (For a more detailed account of the methodology of mental simulation, see Gordon 1992.) Until and unless children develop the capacity and the motivation to make these imaginative adjustments, we should expect them to explain and predict as if everything they themselves count as fact were accessible to the other as a basis for action and emotion. We should also expect them to allow no false propositions into the other's data base: no false beliefs, in other words. Because people with autism are in general severely deficient in the capacity for pretense, particularly other-regarding pretense, they would be unable to make the adjustments posited by the simulation theory. Therefore, the theory predicts, correctly, that these people will generally not succeed in the false belief tasks, even where in other respects their intelligence is normal. Pretending and the "Theory of Mind Mechanism" We argued earlier that the theory-theory is hard put to explain why children with Down's syndrome, who are generally poor theorists, have far more psychological competence than relatively intelligent children with autism, who are generally good theorists. The simulation theory would explain this in part by the fact that children with Down's syndrome, though poor theorists, spontaneously engage in complex, interactive forms of pretend play; whereas children with autism, though often good theorists, do not spontaneously engage in such play. But unlike the simulation theory, the theory-theory does not hold psychological competence to depend on a capacity for certain kinds of pretending. A further move, however, is available to theory-theorists. They may argue that a theory of mental states differs in fundamental ways from theories in other domains, particularly in the nature of the concepts it employs. For one thing, it is a theory of intentional states, of states that are about something. And it may be suggested that possession and use of a theory of intentional states requires a special cognitive mechanism, and perhaps further that the same special mechanism is needed for pretense. This is proposed by one theory-theorist, Alan Leslie, who posits a special computational mechanism, which he dubs the "Theory of Mind Mechanism," as requisite for overt pretend play as well as the understanding and recognition of intentional states (Leslie 1987; Leslie & Roth 1993). This proposal would parallel the simulation theorist's suggestion that both are implemented by "off-line" processing: utilizing systems that are normally dedicated to perception, cognition, motivation, emotion, and decision-making, but using them in at least partial isolation from their normal input and output systems. The simulationist's idea is that the partial independence from input systems would explain, among other things, the freedom we have, in pretend play and in our representation of the content of others' mental states, to portray the world in contrary-to-fact ways; yet, because output systems are not engaged in the normal way, this free play goes on within a "protected" context in which some of the normal consequences, especially but not only some of behavioral consequences, do not actually ensue. Leslie maintains that it is the Theory of Mind Mechanism that makes this protected free play possible. What the mechanism does (to give a greatly simplified account of a rather complex theory) is to enable these systems to function at a higher semantic level: instead of manipulating object-level representations, as in their normal engagement with the world, they are enabled to manipulate representations of representations, or "metarepresentations." The chief matter at issue between Leslie's hypothesis and the off-line hypothesis of the simulation theorist would seem to be this: Do our systems operate at this higher representational level in pretense and in mental state attribution, or do they operate in much the same way as in real-world engagements, but off-line? We believe Leslie's answer misrepresents the nature of pretense: the recognition and understanding of pretense might arguably involve metarepresentation, but not, ordinarily, the production of pretense. We also think the off-line hypothesis explains more, requires fewer specially dedicated resources, and comports better with evidence from other domains, such as imitation and mimicry. Although mimicry is discussed briefly in the following section, detailed discussion of Leslie's hypothesis would not be appropriate in a short essay on autism. We intend to discuss the hypothesis elsewhere, because it appears to be the only way the theory-theory can be squared with the evidence that in the populations tested, psychological competence is better correlated with capacity for pretense than with capacity for theoretical understanding. Simulation and Imitative Behavior The capacity for simulation involves not only the deliberate procedure of "putting oneself in the other's place" but also a number of automatic, unconscious responses. For example, there is subliminal muscular mimicry of the bodily postures and especially the facial expressions of others. Where the other's face bears an expression of emotion, adoption of a similar expression tends to produce a similar emotion in oneself. Even when it does not produce a like emotional response, it at least gives the simulator the wherewithal to recognize the other's emotion. The automatic response to facial expressions is complemented by another mechanism. Like many other animals human beings have an automatic tendency to direct their eyes toward the target of a conspecific's gaze. This mechanism automatically turns one's own attention from the other's response to its environmental stimulus: to the "object" of the other's attention or emotion (what it is about), or the "object" (aim, goal) of the other's action. The tendency is activated particularly when another exhibits startle, terror, or some other strong reactive emotion, or shows attentiveness and interest. In normal children, all of this emerges in the first year. If psychological competence essentially depends on a capacity to simulate others, these imitative mechanisms prove to be important, perhaps even essential, steppingstones to competence. In particular, they facilitate finding the environmental explanation of another's action and emotion. In the case of children with autism there is strong evidence that at least the gaze-tracking response is largely absent and some evidence of deficiency in the tendency to mimic emotional expression. (Baron-Cohen & Ring 1993; Meltzoff & Gopnik 1993). Thus we should expect these children to be deficient in both the tendency to search for reasons for (or objects of) action and emotion and the capacity to locate them in the environment. These problems are not likely to show up in the artificial tasks presented in most false belief experiments, which call primarily for predictions of action rather than explanations. Furthermore, they offer the subject only a narrative rather than a live, expressive protagonist. It is no surprise, then, that in the specific behavior tested in those experiments, the autistic individual seems for the most part to resemble a normal 3-year-old. But where the task is one of explaining another's behavior in terms of an environmental stimulus or "object," and the subject is allowed to see the other's facial expression or overt behavior and track the direction of the other's gaze, the simulation theory predicts that children with autistism will perform far below the level of normal 3-year-olds. Conclusion. We claimed that the evidence suggests that the psychological competence that normal children develop but autistic children do not develop is based not on a theory but rather on a skill. That skill, it appears, includes a capacity for egocentric recentering and a capacity to be engaged as an agent in a world imagined to deviate somewhat from the actual world. These capacities appear to be intact in children with Down's syndrome but deficient in children with autism. Also deficient are some of the ancillary imitative mechanisms that would ordinarily facilitate simulation, particularly by producing emotional responses that copy those exhibited by others and by turning the simulator's attention toward the environmental causes and "objects" of others’ emotions and actions. It should be remarked that this is the first philosophical paper we know of on the topic of autism. We have tried to bring to bear some recent philosophical thinking about the nature and acquisition of mental concepts and the nature of pretense. But we acknowledge that this is at most a small contribution toward understanding what is still a mysterious pathology. Acknowledgements The authors are indebted to Simon Baron-Cohen and Paul Harris for comments that were extremely helpful, especially in filling in some of the gaps in our knowledge of recent empirical research. Baron-Cohen kindly furnished preprints of some of the papers since published in Baron-Cohen, Tager-Flusberg, and Cohen 1993. We thank the Editors for a number of suggestions that helped shape our presentation. [1]We prefer to speak of the child's "psychological competence" rather than the child's "theory of mind," to minimize the danger that descriptions ofthe phenomena to be explained will be skewed by intuitions associated with the term theory.

Deaf people seem to hear signing (Areas in auditory cortex stimulated by sign language in deaf persons) When most people hear sounds or speech, the messages are processed in the auditory cortex, a part of the temporal lobe of the brain. A portion of this auditory cortex is activated in deaf people when they interpret sign language, Japanese scientists assert in the Jan. 14 Nature. Hiroshi Nishimura's team at Osaka University Medical School in Suita City used positron emission tomography (PET) to measure brain activity in a person who had been deaf since birth. First, the person was shown a still picture of someone signing a word. This elicited little activity in the auditory cortex. Researchers then played a motion video of a person signing many words. A part of the auditory cortex called the secondary region was activated in the deaf person watching the video. The individual then underwent surgery to receive a cochlear implant, which permitted some hearing. When the researchers played a sound, PET tests revealed that the primary region, but not the secondary region, of the patient's auditory cortex was activated. The patient was also shown a video of a person's hands moving in a meaningless way. This activated the visual cortex, a separate area of the brain, but not the auditory cortex. These tests suggest that a deaf person's brain changes to make use of the auditory cortex's secondary region for processing sign language. The primary region of the auditory cortex is reserved for hearing sounds, the researchers propose. Pathways: information on the higher auditory system. Frank E. Musiek Pathways is a series in The Hearing Journal related to the higher auditory system. The emphasis is on (central) auditory processing, neuroaudiology, and neurobiology of the central auditory nervous system. One of the key reasons for Pathways is the marked increase in interest in the evaluation and management of auditory processing disorders (APD) and related issues. This increased interest has raised many questions, especially in regard to the application of central auditory tests and management approaches to various clinical populations. A FACULTY OF EXPERTS The experts represent a wide array of disciplinary and professional interests in the central auditory nervous system. In addition to offering diagnostic and management perspectives on APD, offers insight pertaining to the relationships among APD and attention, memory, language, and educational issues. Another topic is the role of amplification in clients with central auditory problems. This topic is of particular relevance given that elderly people comprise the majority of hearing aid patients and also are likely to have experienced changes in the central nervous system. Emerging interest in auditory training as a management course for APD has garnered much attention because of its obvious link to brain plasticity--another topic of contemporary interest. Brain plasticity has emerged recently from the neuroscience literature. The concept of plasticity relates to many aspects of audiology-- especially in regard to auditory training for APD and also training after cochlear implant surgery. BEYOND AUDITORY PROCESSING Beyond auditory processing, we hope to explore current issues in neuroaudiology, the subspecialty of audiology that focuses on dysfunction of the auditory nervous system, beginning at the auditory nerve and progressing along the central auditory system. One obvious topic for discussion is auditory neuropathy. While auditory neuropathy has become a relatively commonly used term, its boundaries and specifics may be unclear to many clinicians. A common question concerns the difference between certain types of central auditory problems and auditory neuropathy. Another topic for discussion is acoustic tumors, as there is always interest in the diagnosis of this disorder and in its rehabilitation. It seems that the focus of acoustic tumor diagnosis and surgery has changed over recent years with more conservative approaches becoming popular. It is our firm belief that most questions posed about APD or neuroaudiology will, in one way or another, refer back to the basic science of the auditory nervous system. Therefore, we will include comments and discussion based on the neurobiology of the system whenever possible. Information derived from functional imaging approaches has generated many new theories regarding the neuroanatomy of the human central auditory system. The study of neurotransmitters of the brain is another area that presents a variety of approaches for understanding neural communication and auditory processing. Though much remains unknown, the potential for significantly impacting the field of hearing rests with neurochemical approaches to underlying auditory mechanisms. The physiology of the central auditory system remains the keystone of learning about audition. From single neurons to an entire system, new electrophysiological techniques are allowing a better understanding of how we hear. Questions that are posed in a practical manner sometimes have far-reaching neurobiologic aspects. We will try to elucidate these relationships whenever possible. Auditory processing provides an excellent opportunity to examine the interdependent relationships between science and clinical practice. Frank E. Musiek, Phd, is Professor and Director of Auditory Research, Department of Communication Sciences, University of Connecticut. He is the author of numerous articles and book chapters related to neuroanatomy and neurophysiology and co-authored or co-edited the books Central Auditory Assessment: Foundations in Clinical Correlates, Neuroaudiology: Case Studies, Central Auditory Processing: New Perspectives, and The Efferent Auditory System.

Treating children with speech and language impairments: six hours of therapy is not enough James Law About 5-8% of children under the age of 5 have developmental impairments of speech and language. This proportion is higher than that for any other neurodevelopmental condition occurring at that age. Parents are concerned about these impairments, and the number of children being referred to speech and language therapy services is increasing. These impairments are characterised by a low level of speech and language skills. Such difficulties may occur secondary to disabilities such as cerebral palsy, sensorineural hearing loss, or autism. Impairment may also be the main symptom in a constellation of comorbid difficulties, such as challenging behaviour or otitis media. Although spontaneous remission of symptoms in primary speech and language disorders sometimes occurs many children will experience long term effects from these disorders. Studies of samples of children from different communities show that children who are at the extreme ends of the distribution of speech and language impairment are at risk of developing problems that can persist into adulthood. The inability to communicate with peers can have a marked effect on wellbeing. Given what we know about the stability of speech and language impairments across time, what role can intervention play? There is evidence to suggest that some interventions can modify intelligence, and the literature about the Head Start programmes in the United States has shown that preschool programmes have a long term impact in terms of social outcomes (for example, in reducing the incidence of teenage pregnancy or incarceration). Clinical experience suggests that speech (whether difficulties involve dyspraxic--that is, neuromotor--or phonological presentations) and vocabulary can be modified but that it is much more difficult to change elements of syntax and verbal comprehension. At first glance the picture painted by Glogowska et al in this issue of the BMJ (p 923) is gloomy. Interventions for speech and language impairments do not seem to work. However, there are some features of this study that should be interpreted cautiously. On average the children spent just six hours with their speech and language therapist in 12 months. How long would it take most people to change their speech and language behaviours? More than six hours, we would argue, even if clients were highly motivated. It is particularly important to note that both groups of children in the study (those who were given therapy and those who were not) continued to have marked language difficulties. This study also needs to be set against a recent systematic review of studies of speech and language impairments that identified effect sizes for randomised and quasi-experimental study designs on the order of one standard deviation. This corresponds to a shift from the 25th to the 5th centile: a good improvement by any standard. These studies all included children of comparable ages and levels of language impairment. The source of the difference provides a potential explanation for the findings of Glogowska and colleagues. All of the studies in the review offered more treatment In many cases the studies were carried out in university clinics and could best be described as efficacy rather than effectiveness studies. On the other hand, Glogowska et al's project is a study of the routine clinical services that are currently available to children in the United Kingdom. INFLUENCES ON INFANT SPEECH PROCESSING: Toward a New Synthesis. Janet F. Werker To comprehend and produce language, we must be able to recognize the sound patterns of our language and the rules for how these sounds "map on" to meaning. Human infants are born with a remarkable array of perceptual sensitivities that allow them to detect the basic properties that are common to the world's languages. During the first year of life, these sensitivities undergo modification reflecting an exquisite tuning to just that phonological information that is needed to map sound to meaning in the native language. We review this transition from language-general to language-specific perceptual sensitivity that occurs during the first year of life and consider whether the changes propel the child into word learning. To account for the broad-based initial sensitivities and subsequent reorganizations, we offer an integrated transactional framework based on the notion of a specialized perceptual-motor system that has evolved to serve human speech, but which functions in concert with other developing abilities. In so doing, we highlight the links between infant speech perception, babbling, and word learning. INTRODUCTION What is remarkable about an infant's ability to successfully process the sounds of speech? The act of perceiving auditory speech represents a difficult and complex computational task. In written speech, each individual letter has its own form; there are spaces between words, and punctuation marks are used to indicate divisions into phrases, sentences, and paragraphs. Although we also think of spoken speech as linear and composed of discrete elements, the acoustic wave form shows no clear boundaries between individual phonemes (a basic sound unit, or phone, used in a language to distinguish one word from another) or between individual syllables, or even words. Moreover, the acoustic cues that signal the beginning of a new phrase or sentence are only probabilistic at best. Yet to perceive (and eventually produce) one's native language, it is essential that an infant not only successfully isolate and segment the individual units in the stream of speech, but that she also represent in some way the information that specifies the regularities among various productions of the same phoneme or word and ignore irrelevant variations. During the past 30 years, researchers have focused on trying to understand how infants begin to solve the complex computational task of speech processing (for a review of common methods used to test infant speech perception, see Werker et al 1998a). We know that infants begin life with a number of perceptual-motor biases that allow them to "break into" the stream of speech, pull out and represent its units, and eventually map sound to meaning. As well, it is apparent that acoustic and phonological cues in spoken speech provide probabilistic information as to the boundaries of linguistic units, and that infants are well designed to detect and utilize this probabilistic information. Finally, researchers are beginning to identify the developmental achievements that allow infants to use the different kinds of information in the stream of speech in their elaboration of language-specific sensitivities.

Changes in retina linked to poorer cognitive function, dementia Stroke: Journal of the American Heart Association Abnormalities in tiny branches of retinal blood vessels might serve as an early warning system for dementias associated with Alzheimer's disease, stroke, and other diseases, researchers report in Stroke: Journal of the American Heart Association. In the study of more than 8,000 middle-aged people who had not suffered a stroke, those with impaired mental function were about three times more likely to have abnormalities in the retinal vessels, called arterioles. "There has been a hypothesis for some time that some vascular cause other than the aging process itself was associated with Alzheimer's and stroke," says Tien Yin Wong, M.D., M.P.H. "This study shows that people with cognitive dementia are more likely to have pathological changes in the retinal vessels, which may be a reflection of similar pathological changes in the brain." Retinal examination could potentially provide an inexpensive, noninvasive way to diagnose and evaluate vascular dementia in the general population, says Wong, a researcher and professor of ophthalmology at the Singapore National Eye Center and National University of Singapore. Previous research by this group found that retinal abnormalities predict stroke independently of traditional risk factors. The study was funded in part by the National Heart, Lung, and Blood Institute.

Medical Acupuncture in the Treatment of Chronic Stress-Related Illness Martha M. Grout, MD, MD(H), FAAMA, FACEP Stress related illness can be defined as any illness whose root cause can be attributed to chronic excessive release of stress-related neurotransmitters. Such illness can include common problems such as anxiety, depression, irritability, insomnia, hypertension, stroke, myocardial infarction, irritable bowel syndrome, as well as less clearly medically defined problems such as chronic fatigue syndrome, fibromyalgia, and even auto-immune diseases. The neurotransmitters and neuropeptides are the biochemical messengers through which information is transmitted or translated from the mind to the body and back.1 Body-Mind Communication Neurotransmitters include not only the commonly known stress molecules (epinephrine, norepinephrine, dopamine and corticosteroids), but also a host of others neuropeptides, short chains of amino acids present in both brain and body cells, with specific receptors on the cell membranes. Recent research shows that almost all communication between different parts of the body occurs by means of this psychosomatic network, a host of neurotransmitters, immunotransmitters, hormones and other chemical substances found in many different tissues in the body. Dr. Candace Pert calls these neuropeptides "molecules of emotion."2 We have neuropeptide receptors all over our bodies, including the gastrointestinal tract; the white blood cells; the kidneys; and the pancreas, giving scientific validation to the ancient Chinese understanding that we feel emotions in all of our elemental organs, although the emperor organ, the heart, is the only one that consciously experiences the emotions. According to Dr. Ernest Rossi, a noted hypnotherapist and student of Milton Erickson, "The autonomic, endocrine, immune and neuropeptide systems are communication channels whereby mind may activate genes and the internal cellular machinery."3 Cholecystokinins in the GI tract, immunotransmitters in nerve cells and white blood cells, and insulin in the pancreas (the middle burner, the solar plexus chakra, the source of our power in relationships) all have receptor sites in the brain. When we experience a particularly trying event, the memory is encoded by means of unique combinations of these chemical transmitters. If the memory is too painful for our conscious minds to deal with, it may be stored (and effectively buried) in particular places in our bodies. As long as the memory is still encoded in the body, it may try to bring itself to our attention by causing pain, dysfunction or imbalance in that place where it was stored.4 Consider, for instance, the patient with chronic neck and back pain, unresponsive to standard therapies and only partially responsive even to acupuncture. Needling a particular place on the neck brought to the surface memories of a five-year old being grabbed by the neck by his father, with the attendant feelings of "I didn't do anything! I am small and powerless! It's not fair." This patient had encoded that memory in the part of the body related to the upper burner, the lungs, whose associated emotion is grief, and which is concerned with structure and rules, justice and duty; and the heart, where that emotion is experienced. Once the memory was released and the father was forgiven, the physical pain was completely relieved. How Can Acupuncture Help? First, we can diagnose the medical illness, imbalance or problem that brings the patient to us. We are obligated to use our Western diagnostic skills and modalities, to determine whether we are dealing with a functional illness; with something that is surgically correctable; or even a life-threatening condition like pneumonia, sepsis, diabetic ketoacidosis or cancer. Second, we can diagnose the energetic imbalance, using the system to which we best relate. We may use five-element diagnosis,5 French energetics6 or traditional Chinese medicine syndromes.7 In the end, if we diagnose correctly, we will all come to the same conclusions about the imbalance, although our plans of treatment may be different, depending on which system we are using. Third, we treat the whole person: body, emotions, mind and spirit. Treatment If the disease or problem exists primarily on the emotional level, then our acupuncture treatment is directed at this emotional level, as well as the physical level. I find that the outer bladder line points are most helpful in this regard.8 I use BL42 (pohu) as well as the lung shu point BL13 (feishu) for patients with Valley fever or asthma, in which the root cause is likely to be an issue of enormous grief. Similarly, I use BL47 (hunman) and the liver shu point BL18 (ganshu) for patients with hepatitis, where the cause is rooted in emotions of anger or irritability. The gallbladder shu point BL19 (danshu) is combined with BL48 (yanggang) for patients with gallstones or cholecystitis, where is root issue is repressed anger and lack of courage to move on. I also activate the fu organs themselves for their metaphorical functions. Issues of irritability may express themselves in the stomach as ulcers or gastritis, with the emotional issue revolving around "What is there that you cannot stomach?"9 The stomach mu point CV12 (zhongwan) and the shu point BL21 (weishu) are most helpful for treatment of these issues. I frequently use the small intestine mu point CV4 (guanyuan) or the shu point BL27 (xiaochangshu) for people who are unable to clarify the issue, "What is there that you cannot sort out?" and whose manifestations tend to be bloating or irritable bowel syndrome. The large intestine mu point, ST25 (tianshu) and shu point BL25 (dachangshu) are very useful for those patients who are unable to let go of that which no longer serves them. They tend to have issues of forgiveness, and manifestations of chronic constipation or colitis. If the problem lies in the patient's fundamental mindset ("I am not worthy," "I am ugly," "I do not deserve the good things in life") as often occurs in cases of childhood neglect or abuse, it is important to work with the mindset as well. Abuse may not necessarily mean gross neglect; it may be as simple as Mom being preoccupied with a new baby, or Dad being chronically disappointed because we got Bs rather than As in school. The cerebral circulation pathways10 are particularly helpful for such core "mindset" issues of worthiness. These pathways are based on a combination of French energetics, anatomy and molecular biology. The yin channels of the leg - tai yin spleen, shao yin kidney and jue yin liver - originate from cephalad points on the three leg yin meridians, and continue their influence deep into the brain, connecting eventually with the yang channels of the leg in the head, yang ming stomach, shao yang gall bladder and tai yang bladder, which run superficially over the head and face. The cerebral circulation pathways, arising from the cephalad points, influence the sensory organs associated with the three yin meridians, as well as the associated emotional states. The kidney cerebral circulation is activated from KI27 and is focused on SI19 (tinggong) for the ear, or on BL10 (tianzhu) for the posterior pituitary gland across which the channel travels. The pituitary gland is the great controller of our endocrine organs, secreting vasopressin or anti-diuretic hormone, which regulates water balance, blood flow and urine flow. This pathway is useful in any ear problem as well as any endocrine problem, and is particularly useful for those patients whose primary issue is that of fear of change; fear of relationships; or fear of living in general. The liver cerebral circulation is activated from LR14 (qimen), and is focused on GB1 (tongziliao) for the eye or on GB20 (fengchi) for the anterior pituitary gland. The anterior pituitary gland secretes luteinizing hormone, which is used in lactation; follicle stimulating hormone, which regulates the ovaries, and ACTH (adrenocorticotropic hormone), the precursor of beta endorphins and enkephalins.11 Stress-like behavior, memory, attentiveness and learning are all mediated through the adrenal glands. This pathway is especially useful in people with attention deficit hyperactivity disorder, who clearly exhibit characteristics of liver wind (darting about and being unable to focus clearly). This pathway is also useful for our hypertensive chronically irritable patients, as well as those with refractory eye problems such as glaucoma and macular degeneration. This pathway is particularly useful in the treatment of those patients who are crippled by their irritability and anger, or who spin their wheels and never move forward. The spleen cerebral circulation is activated by the highest point on the spleen meridian, SP20 (zhourong). It ascends through the pharynx to the maxillary sinuses and olfactory bulb. The focusing point is ST1 (chengqi) for the sinuses; BL1 (jingming) for the nose; and ST9 (renying) for the throat. The extra meridian point GV24.5 (yintang) can also be used for both olfactory and sinus problems. This may be very useful in treating chronic sinusitis that has been unresponsive to other less aggressive treatments. Since the spleen is charged with both logical thinking and intuitive thinking (through the nose), this pathway is also useful in treating patients with confusion and memory dysfunction, and those who have suppressed their intuition, who live "all in their heads" and are excessively logical. It is especially useful for those who get gridlock or stagnation on any level, those who have obsessive-compulsive disorder, and chronic worriers. Conclusion Medical acupuncture is extremely useful in the treatment of many chronic stress related illnesses, not only because of its effectiveness in treatment of the physical body, but also (and perhaps more importantly) because of its ability to penetrate the layers of defense and coping mechanisms which our patients exhibit. Once the defenses are penetrated, the patients have the opportunity of choosing to deal differently with their issues. Since, as we have demonstrated, the mind and the body are one inextricably connected entity which uses the emotions and their attendant neuropeptides as the vehicle for communication, it is clear that by treating the physical body, we can penetrate deeply into the emotions. By releasing the emotions, we can help our patients change their response to stress, and thereby enable them to heal that physical entity known as the body-mind. Acupuncture as Stroke Medicine? (HealthScoutNews) Researchers are trying to see if acupuncture can poke away at the debilitating effects of stroke. A pilot study to compare the effects of real acupuncture to sham acupuncture in treating stroke patients is being conducted by researchers at the New England School of Acupuncture, Massachusetts General Hospital, Spaulding Rehabilitation Hospital, Harvard Medical School and Harvard School of Public Health. Computerized imaging of gait and limb movements and magnetic resonance imaging (MRI) of the brain will be among the methods used to evaluate potential acupuncture benefits. "This study will look at a number of clinically driven questions about how effective acupuncture can be in reducing some physical impairments, removing functional limitations and enhancing the quality of life in patients with chronic hemiparesis," says principal investigator Dr. Peter Wayne, director of the acupuncture school. Hemiparesis is weakness or paralysis on one side of the body, and is the most significant chronic effect of stroke. For the study, researchers are looking for people who have had a stroke at least six months earlier, and still experience weakness on one side of their body. Participants are being recruited through Spaulding Rehabilitation Hospital. This year, an estimated 750,000 Americans will suffer a first or recurrent stroke. That works out to a stroke every 45 seconds. Stroke is the leading cause of adult disability.

The Society for Neuronal Regulation's 10th Annual Conference took place in Scottsdale, Arizona September 12-15. The abstracts below were presented at the conference. We thought you would like to know some of the very latest research. -The Crossroads Institute- EEG and Intelligence M. Doppelmayr, PhD and W. Klimesch, PhD University of Salzburg, Department of Physiological Psychology, AUSTRIA michael.doppelmayr@sbg.ac.at Introduction. Since the pioneering work of Hans Berger, there have been many attempts to find electrophysiological correlates of intelligence by using a variety of different measures which in most cases were based on event-related potentials (ERPs). Method. We report findings from a different approach which is based on the analysis of small frequency bands that are dynamically adjusted to individual alpha frequency and bandwidths (Doppelmayr, Klimesch, Pachinger, & Ripper, 1998). Previous work indicates that increasing demands on working memory are associated with an event-related increase in theta band power whereas increasing demands on semantic (long-term) memory are reflected by a selective decrease in upper alpha band power (Klimesch 1997; 1999). Findings. Based on a similar methodological approach Neubauer, Freudenthaler and Pfurtscheller (1995) and Neubauer, Sange, and Pfurtscheller (1999) have obtained interesting results with respect to intelligence. As an example, they have found that the extent of decrease in upper alpha power (event-related desynchronization or ERD) is negatively associated with intelligence: More intelligent subjects exhibit a smaller ERD than less intelligent subject. This finding was interpreted on the basis of the 'neural efficiency' hypothesis. In a recent study from our laboratory (Doppelmayr, Klimesch, Stadler, Pollhuber & Heine, 2002) we have found different effects for the lower and upper alpha band in a resting situation with respect to the performance of tasks with high demands either on attentional or long-term memory processes. Whereas intelligence tasks with high attentional demands (such as the LGT-3) selectively affected the lower alpha band, those with high demands on long-term memory (such as the IST-70) primarily affect the upper alpha band. These findings could be replicated and extended by analyzing the EEG while subjects were performing a combination of the Ravens Standard and Progressive Matrices. Analyzing task performance according to an additional intelligence test (CFT-3) and the amount of band power changes for individually adjusted frequency bands and bandwidths revealed several significant results for different time segments, frequency bands and topographical positions. Discussion. The findings of the different studies show several significant differences in band power changes between higher and less intelligent subjects, mainly in the alpha bands. While the results underline the different functional meaning of specific frequency bands as reported by Klimesch (1999) not all of the findings of Neubauer et al. (1999) could be replicated. The results will be discussed in detail with respect to the neural efficiency hypothesis. Neurofeedback with Obsessive-Compulsive Disorder D. Corydon Hammond, PhD Professor, University of Utah School of Medicine, Salt Lake City, Utah D.C.Hammond@m.cc.utah.edu Introduction. Obsessive-Compulsive Disorder (OCD) is often less than optimally treated using medication or behavior therapy. However, qEEG and neuroimaging research have identified brain patterns associated with OCD (Prichep et al., 1993). Method. Two patients with OCD were screened with the Padua Inventory, the Yale-Brown Obsessive-Compulsive Scale, qEEG, and in one case, the MMPI. Each patient displayed different qEEG patterns associated with OCD. Neurofeedback individualized to qEEG findings was used. Results. At the conclusion of treatment, the two patients were again administered the Padua Inventory, and an independent colleague conducted the structured interview associated with the Yale-Brown Scale. The MMPI was also administered again. These results and follow-up questioning at four months and more than one-year post-treatment validated highly successful changes. Conclusion. EEG neurofeedback appears to hold promise for treating OCD, which has been firmly established to be associated with abnormal brain patterns QEEG/ERP/ERD Based Diagnosis and Biofeedback Treatment of Executive Dysfunction Juri D. Kropotov, PhD Institute of the Human Brain of Russian Academy of Sciences, St. Petersburg, RUSSIA kropotov@ihb.spb.ru Introduction. Attention Deficit Hyperactivity Disorder (ADHD) is the most common mental dysfunction in childhood, affecting three to five percent of all children. It is not a homogeneous disorder. A modern neurobiology oriented approach considers ADHD subtypes to be associated with the impairment of different neuronal circuits in the frontal lobe-basal ganglia-thalamic executive system. Method. To differentiate between impairments of different executive operations (engagement and disengagement operations, in particular) we measured event-related de-synchronization and late (in the range of 300 ms after stimulus) positive GO and NOGO components of event-related potentials (ERPs) associated with engagement and disengagement operations in a continuous performance task in normal (N=16) and ADHD (N=84) groups. Results. Our data show that the extent of event related desynchronization in alpha band, of event-related synchronization in theta band, as well as the amplitude of GO an NOGO components correlate with both age and task performance. They are smaller in young children in comparison to older ones, and in the ADHD group in comparison to the normal group. Twenty sessions of beta EEG training improved the quality of performance (decrease of omission and commission errors) and led to a significant increase of amplitude of GO and NOGO components as well as to normalization of event-related synchro/desynchronization. Conclusion. This study is the first to show that not only psychological indexes of behavior, but also ERP/ERD components are “improved” after beta training, which in turn indicates that the biofeedback training changes the brain system for executive function.

High carbs vs. high fats: This is the real food fight Healthy News It's the diet industry "smackdown." In one corner stand the high-carb, low-fat legions, those who will eat a plate of pasta but, please, no butter and oil. In the other are those who will gorge on bacon, eggs and red meat, but won't touch a slice of bread or a bowl of rice. High carbs and low fats vs. high fats and low carbs. It's a renewed food fight, one that is pulling in more and more nutritionists, scientists and cardiologists. The impetus: Over the past decade, coinciding with the release of the carb-friendly Food Guide Pyramid, we've gotten fatter than ever. Some experts blame a sedentary lifestyle. Others point to Texas-size portions. Some are contending the problem intensified in 1992, when the U.S. Department of Agriculture created the Food Guide Pyramid. It was built on the premise that bread, cereal, rice and pasta should define the diet. Critics contend that in recommending carbohydrates, the pyramid made the mistake of lumping simple carbohydrates like fructose or glucose, with virtually no nutrients, and complex ones, which contain fiber and minerals. So when Americans were told to eat bread, few distinguished between processed white bread and fiber-rich whole grain. Carbohydrates will always be the body's main source of energy, but if you consume more carbs than you release energy (it's obesity that's rising, not exercise rates), the leftover carbs become stored fat. As a result, more doctors today are recommending a low-carb diet. The undisputed captain of the low-carb movement is cardiologist Robert Atkins. In 1972, he released his "Diet Revolution," promoting a diet so high in fats and so low in carbohydrates that many nutritional associations declared him a health hazard. Now some are taking a second look. His hypothesis says that carbohydrates may have fewer calories than fat, but they make the eater hungry again much more quickly. "Fat satiates the appetite. Fat stops carbohydrate craving. And fat, in the absence of carbohydrates, accelerates the burning of stored fat," Atkins wrote in his 1992 update, "New Diet Revolution." The American Journal of Medicine published a study of the Atkins diet undertaken at Duke University Medical Center (and funded by the Atkins Center for Complementary Medicine). The study indicates that a low-carb diet can lead to significant weight loss. Eighty percent of the 50 who adhered to the diet lost an average of 10 percent of their original weight; average loss per person was 20 pounds. The six-month study is just preliminary research, and Eric Westman, principal investigator of the study, says he is not confident about the safety or long-term success of the diet. But Rita Miller, 49, president of the Broward chapter of the Florida Dietetic Association, tried the Atkins diet at age 19 and still regrets it. Miller lost about 15 pounds but suffered other health problems. "Biochemically, our bodies were not intended to only eat protein and fat," Miller says, voicing the long-standing medical objections to the diet. "Anyone who is on the Atkins diet has horrific constipation, which can lead to colon cancer. Another issue is the more protein you eat, the more calcium you lose; the more protein you consume, the harder your kidneys have to work." Rather than burning glucose, people on the Atkins diet undergo ketosis, in which the body burns fat for energy. Critics contend that muscle mass also can be burned, but Atkins says that sufficient protein intake prevents that. Barry Sears, author of another popular diet called "The Zone," says he is happy scientists are re-evaluating the Food Guide Pyramid because of what he calls its failure to account for appetite-triggering insulin response. Sears' plan is neither low carb nor low fat. A typical "zone" meal divides the plate into three sections. On one-third, put a piece of low-fat protein no bigger than the palm of your hand. The others you fill with fruits or vegetables and a dash of fish oil -- fish oil has omega-3 fatty acids (good fat), and research shows that omega-3s are heart protective. According to Sears, that meal will keep your insulin level stabilized for four to six hours. Good Fat, Bad Fat, The Choice Is Yours Healthy News LAST week we looked at dietary excess and today we examine the other side of the story, where the opposite is true; when too little dietary fat can contribute to health issues, including overweight. An enormous amount of media attention has recently been given to fat. Much confusion surrounds the topic and just how much and what types of fat are required each day. And the answers can be just as confusing with the range of information available. The 1980s saw the advent of yet another change in dietary advice for the masses. The overall message was that fat was bad for your body weight and bad for health in general. As the 90s progressed, the message started to change and it was the type of fat that really mattered. It was OK to eat vegetable fat but not animal fat, yet the overall message of fat minimisation still held true. The word fat covers a number of different types of fat. Saturated fat is primarily of animal origin and has been implicated in number of the lifestyle diseases yet it contributes to an important immune response. Monounsaturated fats are primarily found in olive oil, avocados and macadamia nuts and have been demonstrated to have an enormous range of health benefits. Polyunsaturated fat falls into two categories: omega 6 and omega 3. Some of these are essential fats; that means our body cannot make them, we must eat them. Omega 6 polyunsaturated fats have been demonstrated to have heart health benefits and are widely found in many vegetable oils, seeds and nuts, while the omega 3 fats, commonly found in fish and linseed are excellent for a range of health issues including blood pressure, cholesterol problems and inflammatory conditions such as rheumatoid arthritis. Hence, a balance of all of these fats in your diet is important. One of the problems with the changing messages has been those who take dietary information to the extreme. Within the general population are those who decided that if a low fat diet was good for your health, then a no fat diet must be even better. And that is simply not the case. Fat is vital for good health. Whether you are seeking to optimise your health for disease prevention, feelings of well-being or sporting performance, the appropriate fat intake is an integral component of a balanced diet. Fat is important for skin, hair and vision and it makes vital contributions to your immune system. Fats contribute to hormone production, to mood and to digestive processes. Without it we would melt! Diets offering blanket advise continue to confuse consumers. We are individuals with different dietary needs and these needs depend on a variety of factors. Current dietary recommendations suggest 30% of the daily energy intake be fat, not 30 grams. For an individual consuming approximately 2000 calories per day (8400kJ), that translates to 70 grams of fat per day. That may sound like a lot if you are used to eating less than 30 grams a day, but you are likely to feel more satisfied eating more fat and therefore, consume the same or less total energy over a day. As you read last week, it is the total amount of energy (kilojoules or calories) you eat in a day that matters when it comes to weight management. If you are used to eating a no fat or very low fat diet, eating the right amount of fat for you may actually assist with weight management and improve your overall health. Omega-3 Fatty Acids May Ease Depression Healthy News You are what you eat ... and your mood could be affected by your diet, as well. For the last decade, researchers and alternative medicine practitioners have been exploring a new, natural way to treat those suffering from depression and other psychiatric disorders. And what they've found is that improving your mood could be as simple as making minor adjustments to your diet. One lead researcher, Dr. Joseph Hibbeln, chief of the outpatient clinic at the National Institutes of Alcohol Abuse and Alcoholism in Bethesda, Md., published a study in 1998 in the journal The Lancet that showed a connection between countries that consume large amounts of fish and low rates of depression. On the other hand, countries where people did not eat a lot of fish had significantly higher rates of depression. This study led other researchers to wonder whether the polyunsaturated fats known as omega-3 fatty acids found in fish could be the reason for the difference. Dr. Andrew Stoll, director of the psychopharmacology research laboratory at McLean Hospital in Belmont, Mass., conducted a study that focused specifically on patients with bipolar disorder. Half of the subjects were given fish oil tablets and the other half were given a placebo. After four months, "half of the placebo cases had already relapsed into depression, where as only two out of the 15 fish-oil patients had gotten sick, and that was a huge difference," says Stoll. The significance of these two studies sparked additional research over the last couple of years that have shown similarly promising results on the ability of omega-3 fatty acids to relieve depression. Getting Enough Omega-3 While additional research needs to be done to prove definitively omega-3s' impact on different psychiatric disorders, some psychiatrists are now feeling confident enough to recommend that their depressed patients increase their consumption of these fatty acids. So, what are the best sources for omega-3s, and how much is needed to make a difference? The best source for omega-3s is any type of seafood -- including salmon, lobster and shrimp. For people who find seafood a bit fishy, walnuts and olive oil are also good sources for the fatty acid. "People should not fall below 650 milligrams [of omega-3] per day," says Hibbeln. "A 100-gram serving of fish on average is going to contain about a gram or 1,000 milligrams of omega-3. So, 650 milligrams is about a serving of fish every other day." However, for most people it may be unrealistic, or unappealing, to eat fish every other day. For those people, doctors recommend fish oil supplements that can be found in any health-food or nutrition store. Additional Effects of Eating More Fish In addition to the possibility of relieving depression, omega-3s have proven to be important in cardiovascular health. Numerous studies led the American Heart Association two years ago to make a recommendation that consuming two to three servings of fish per week could provide significant cardiovascular benefit. Omega-3s have also proved promising in preliminary results for the prevention and treatment of certain cancers, including colon cancer, and with inflammatory conditions, such as rheumatoid arthritis. In addition, pregnant and breast-feeding mothers are encouraged to get enough omega-3 to help the development of their babies' brains. However, some predatory fish like tuna, swordfish and shark may be dangerous to pregnant mothers due to the high levels of mercury. So, sticking with fish like salmon is a safer bet for those expecting a child, without the unwanted effects of consuming mercury. The only reported down side to consuming more of these fatty acids through fish or fish-oil tablets may be an increase in dyspepsia, or indigestion often resulting in gas. "People may get a little bit of dyspepsia, but if they just start with a low dose and work their way up, it shouldn't be a problem," says Dr. Harold G. Koenig, associate professor of psychiatry and medicine at the Duke University Medical Center in Durham, N.C. "That's a fairly mild side effect for all the good things that could potentially result." "Not only are the fish oil supplements relatively inexpensive," says Hibbeln, "and not only are they safe and recommended for pregnant mothers, but all of the side effects, except for belching, are beneficial." The Future of Omega-3s and Depression While the existing results of studies involving omega-3s and depression have proven promising, there still remains skepticism as to how significant the impact will be on the continued need for prescription antidepressant medication. Therefore, further studies need to be done to see which patients will benefit the most from an increase in omega-3s and to see how well this new diet works in combination with antidepressant drugs. But, in the meantime, some psychiatrists are encouraging patients who haven't been successful with the drugs to incorporate this new approach. "For patients who are taking adequate doses of antidepressants, and maybe they tried one, maybe they tried two or three," says Koenig, "then why not encourage them to take this pill that's likely to have a benefit for their cardiovascular system and it might help to stabilize their emotional condition, as well?"

Brain Repair By Donald G. Stein, Simon Brailowsky, Burno Will The key to neuroscience's most exciting discoveries to date is a theory that is rapidly gaining adherents in the scientific community--the theory of neuroplasticity. Neuroplasticity stresses that cells throughout the brain can not only regenerate, but can adapt their function to assume critical roles once performed by damaged tissue. In clear, accessible language, the authors, three renowned neuroscientists review recent advances in the research, technology, and treatment and show us that the brain manufactures a host of complex chemicals that actually foster growth in damaged brain cells. We visit the laboratories where researchers are untangling the mystery of Parkinson's disease and trying to understand what goes wrong in stroke victims, and why some, thought permanently impaired, show remarkable improvements. In addition, they discuss how even today misguided ideas can adversely affect how physicians treat patients. And, along the way, they detail the fascinating history of how brain structure and functioning has been understood and studied, from prehistoric times to the present.

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