Aug 2003


The Crossroads Institute Newsletter


In July Dr. Curtis Cripe and Dr. Martha Grout were presenters at the 11th Annual International Conference on Thinking in Scottsdale, AZ. Their topic was entitled "Attention Deficit Hyperactivity Disorder: A New Paradigm for Treatment."


Initial funding has been secured for a joint research project with the Russian Academy of Science, St. Petersburg, Russia. This project's scope includes studying the effects of the Dynamic Listening System on overcoming auditory related issues. Future plans include studying combined effects of auditory stimulation with neurotherapy.


Dr. Cripe has been asked to participate as a panel speaker at this year's ISNR (International Society for Neuronal Regulation) conference in Houston, Texas. The panel's discussion will center on the advancements in neurotherapy as it relates to PDD.


Dr. Martha Grout is again making plans to travel to China this fall to continue her studies in Chinese Medicine.


ACCELERATED PERFORMANCE


Everyone is somewhere on the Neurodevelopmental Spectrum. Where are you on it .... where do you want to be?

Accelerated neurodevelopment allows us the ability to maximize and use our intellectual, physical, and emotional strengths simultaneously, no matter where we begin on the spectrum.

When accelerating brain power, daily tasks such as working, studying, and sports become easier to do and manage. The brain is functioning at optimal levels and is able to make quick attentional shifts on demand.

This is the state of mind that peak performers call "the zone" and is accessible at will.

NEWS BRIEFS



A way to train the brain: 
Scientists take a systematic look at the benefits of neurofeedback
 
By Jerome Burne
FINANCIAL TIMES 

LONDON, July 11 —  Sitting at a desk on the 10th floor of Charing Cross hospital, Tobias Egner appears to be relaxing with a curious computer game. Shapes keep changing on the screen but there is no mouse or keyboard. Instead, wires trail from different points on his scalp.
   
IN FACT, he is working hard at an activity that most people can keep up for only about 20 minutes. Dr. Egner, of the department of cognitive neuroscience and behavior at Imperial College London, is improving his memory and attention by changing his brain waves. Three leads attached to his earlobes and the top of his head connect to a device that monitors his brain activity. The raw data is “fed back” on a screen so that Dr. Egner can see how his brain activity affects the shapes on the monitor.
       
“We tell users: ‘Just let the feedback guide you — be relaxed but focused,’ ” says David Vernon, his colleague.
       
Studies already show that neurofeedback, as the process is known, could be an effective form of drug-free treatment for alcoholics, epileptics and children with attention deficit hyperactivity disorder.

John Gruzelier, who runs the cognitive neuroscience and behavior laboratory at Imperial, is one of the few U.K. researchers in this field. In the United States, neurofeedback therapy has grown fast, mainly among parents of ADHD children looking for a non-drug treatment.
       
Neurofeedback is based on the fact that our brains produce electrical waves of different frequencies (hertz) that can be recorded with an electroencephalograph. Each is broadly associated with a particular mental state. Beta waves, the fastest, are 15 Hz to 18 Hz, alpha waves 12 to 15 Hz and theta a leisurely 4 to 7 Hz. Beta is linked with day-to-day alertness, alpha with relaxation and theta with imaginative imagery, although too much theta can cause problems — for instance, inducing a dreamlike state that makes concentration difficult.
       
In the 1960s, researchers found that first animals and then people could learn to produce different types of brain waves at will, using feedback, such as a light or a tone. Then a chance observation found it was possible to prevent an epileptic fit, which involves a slow wave of theta rolling across the brain, by learning to produce “sensorimotor rhythm” (SMR) waves, a particular sort of slow beta wave found in a brain region known as the sensorimotor cortex.

Children with ADHD show a different pattern of inappropriate theta — they go into slow theta at just the time they need beta to concentrate — and so benefit from learning how to stay in beta. “There are about five good studies supporting this,” says Professor Gruzelier. “The kid’s IQ goes up and so does their ability to attend [to] and comprehend tasks.” A big randomized trial is under way at Northwick Park hospital in London.
       
One form of neurofeedback, the “Peniston protocol,” has had dramatic results in helping recovering alcoholics. This concentrates on producing a particular frequency where relaxing alpha waves turn into even slower theta.
       
But anybody can benefit. Professor Gruzelier ran a study two years ago in which he showed neurofeedback could significantly “optimize performance” of high-achieving students at the Royal College of Music by encouraging theta waves. His team took videos of students in performance and had them rated by independent experts.

Groups of students were allocated to different therapies including aerobics, Alexander Technique, mental skills training and neurofeedback. After two years the students were filmed again and assessed. All those in the neurofeedback group had improved, some by 50 percent, in “stylistic accuracy” and “interpretative imagination.” The number of incidental errors also fell significantly.
       
This year, Professor Gruzelier, who believes applications are “unlimited,” published a paper that showed that people trained to increase both SMR/beta and theta in combination improved both attention and memory. There is also the attraction that the process looks safe, non-addictive and effective.
       
“Further tests are needed to confirm this,” Professor Gruzelier cautions, “but if neurofeedback can positively influence the cognitive performance of healthy individuals, it opens up the possibility that such treatment may be beneficial for those suffering from cognitive deficits.”
       
© The Financial Times Ltd 2003. "FT" and "Financial Times" are trademarks of the Financial Times.
       
 

       
   
Major Problems With the Vaccine Procedure

By Bronwyn Hancock Vaccination Information Service

We have all been repeatedly told that vaccination is both safe and protective of children against dangerous diseases. Many parents upon learning of adverse effects realize that their trust has been betrayed--that vaccines are not safe at all. However, it is common for them to continue to trust that vaccines are effective and that the diseases they purportedly prevent are dangerous. This creates a terrible dilemma for these parents, who end up feeling that either way they are taking a risk.
However, with more investigation increasing numbers of parents are discovering that nature is not so cruel as to force such a difficult dilemma on them. The full reality is that not only do childhood illnesses (provided they are properly managed) have a priming and maturing role in immune system development rather than being dangerous to unvaccinated children, but also vaccines have never prevented any diseases. Other factors have clearly been responsible for the declines that have occurred, and the very toxic and invasive nature of vaccines that causes the observed adverse effects also makes them counterproductive for their very purpose of protecting against diseases.

Rather than discussing the statistical evidence, false assumptions and misinterpretations relating to the myth of vaccination effectiveness, which are covered by various books and Web sites, what is far less widely known, and what I will cover here, is the actual effect that vaccines have on the immune system, which causes them to be counterproductive.

I must give credit for my awareness of this to Dr. Viera Scheibner, who is arguably unsurpassed in her width of knowledge and depth of understanding of the vaccination issue, having studied over 100,000 pages of medical research on the subject. Having worked closely with her over a number of years, I have read much of the most revealing research that she has uncovered.

There are two main causes of the problem: the toxic nature of the ingredients in vaccines and the invasive form of delivery.

Ingredients, the Injection Process and the Result

At the bottom of this article is a brochure that summarizes the subject and starts with a list of the ingredients in vaccines. In respect to these, first there are those that are poisonous by their very nature regardless of how they are administered such as formaldehyde, mercury, aluminum compounds, phenol, acetone and antifreeze. It is well established that such poisons, even on their own, are immune system SENSITIZERS. This means they make the immune system more sensitive, or less able to cope appropriately with foreign substances that it encounters.

Then there are other ingredients such as animal organ tissue and blood that our bodies would not have a problem with IF they entered the body orally because our digestive system breaks down foreign proteins, unusable in that form, into their constituent amino acids, which are then absorbable and useable by the body.

However, our immune systems have not been designed to deal with foreign proteins being injected. In fact the injection of any foreign substance is well known to suppress the immune system, and vaccination is no exception.

Effects

The immune system becomes derailed and confused, and often even when these proteins subsequently are encountered by a natural portal of entry (e.g. through the digestive system or lungs), the immune system reacts. This of course is what is known as an allergic response. One manifestation of this, asthma, kills over 10,000 people annually in the United States.

Other effects include more serious "atypical" forms of the targeted diseases and a reversed ratio of T4 and T8 cells that characterizes a host of modern immunodeficiencies including autoimmune diseases, cancer (now in the young), chronic fatigue syndrome and AIDS. All of these conditions were unknown before the vaccination era. (See accompanying brochure for a more complete list of vaccination effects.)

Bypassing Vital Defenses

Another problem with the injection process in respect to any viruses and bacteria that are being administered is that very important outer levels of defense are bypassed, giving them deep access into the body to cause damage. Hence, for example, the now well known finding of the vaccine strain of the measles virus in the gut of a significant proportion of autistic children.

It has also been found that animal, bacterial and viral DNA, when injected, can be incorporated into the recipient's DNA. No wonder vaccination has been linked to cancer, particularly considering vaccine ingredients even include animal cancer cells (used for the culturing of viruses because they continue to multiply).

Some Babies Just Cannot Cope

Some babies lose the battle against the invasive toxic assault of vaccination in hours, days or weeks. If the parents are "lucky" it is diagnosed as cot death, or if an organ fails it is classified simply as failure of that organ (e.g. kidney failure). However, if injuries such as subdural hematomas or retinal hemorrhages are found, the parents (or other care-giver) find themselves falsely accused of murder in the form of "shaken baby" syndrome.

Vaccine-Induced Antibodies Do NOT Indicate Immunity

What causes confusion to many medical doctors is that part of the sensitization reaction to vaccination is the production of antibodies. This is falsely equated with the opposite, intended effect, which is to bring immunity. The aluminum compounds are even included for this very purpose (as "adjuvants") to artificially force the production of a significant number of virus-specific IgG antibodies, because the immune system does not naturally produce them (in significant levels) on demand by injections.

However, the IgG antibodies thus produced only show that there has been exposure to that virus. Their presence does not mean immunity. The secretory IgA antibody, which does NOT get produced by injections because injections bypass the outer level processes of the immune system, has been found to be a far better measure of immunity.

This is why contracting tetanus, the well known way being by a deep puncture wound, which is just like an injection, does not bring immunity. The result is even said to be "sensitization" to tetanus in the future. Immunity can develop, however, if the bacteria enter via the natural portals of entry, often without the person even being ill with it. When it comes in through the natural portals of entry it is also in its aerobic form, which does not produce the neurotoxins that cause the characteristic tetanus symptoms such as locked jaw and tetanic spasms.
The fact that some children do not have noticeable adverse effects to vaccination does not mean that for them the procedure is beneficial, it is just that we have great variations.

 



Chronic fatigue syndrome: new evidence for a central fatigue disorder.

Clin Sci (Lond) 2003 Apr 23
Georgiades E, Behan WM, Kilduff LP, Hadjicharalambous M, Mackie EE, Wilson J, Ward SA, Pitsiladis YP.

Considerable evidence points towards a prominent role for central neural (CNS) mechanisms in the pathogenesis of chronic fatigue syndrome (CFS), a disorder characterised chiefly by persistent, often debilitating, fatigue.

We wished to characterise circulating profiles of putative amino acid modulators of CNS serotoninergic and dopaminergic function in CFS patients at rest, during symptom-limited exercise and subsequent recovery.

Twelve CFS patients and eleven age- and sex-matched sedentary controls, with similar physical activity histories, underwent ramp-incremental exercise to the limit of tolerance. Plasma amino acid concentrations, oxygen uptake (Vo 2) and ratings of perceived exertion (RPE) were measured at rest, during exercise and recovery.

Peak oxygen uptake (Vo 2peak) was significantly lower in the CFS patients, compared to controls. RPE in the patients was higher at all measured time points, including rest, relative to controls. Levels of free tryptophan [free Trp];the rate-limiting serotoninergic precursor, were significantly higher in CFS patients at exhaustion and recovery, whereas concentrations of branched-chain and large-neutral amino acids (BCAA and LNAA, respectively) were lower in patients at exhaustion and, for [LNAA], also during recovery.

Consequently, the [free Trp] : [BCAA] and [free Trp] : [LNAA] ratios were significantly higher in CFS patients, except at rest. On the other hand, levels of tyrosine, the rate-limiting dopaminergic precursor, were significantly lower at all time points in the patients.

The significant differences observed in a number of key putative CNS serotoninergic and dopaminergic modulators, coupled with the exacerbated effort perception, provide further evidence for a potentially significant role of CNS mechanisms in CFS pathogenesis.

RESEARCH AND ADVANCEMENTS

Inhibitory circuits in sensory maps develop through excitation

Naoum P. Issa

Trends in Neurosciences, (July 16, 2003), 10.1016/S0166-2236(03)00209-1

Abstract

Inhibitory and excitatory connections are equal partners in determining neuronal response properties. Although the development and plasticity of excitatory networks have been heavily studied, little is known about how inhibitory circuits develop.

In a recent study, Gunsoo Kim and Karl Kandler have shown that, as in the development of excitatory circuits, synapse elimination and strengthening are important processes for the development of well-organized inhibitory circuits.




Hemispheric asymmetries in cerebral cortical networks

Jeffrey Hutsler and Ralf A.W. Galuske
Trends in Neurosciences, (July 07, 2003), 10.1016/S0166-2236(03)00198-X

Abstract

Since the middle of the 19th century it has been recognized that several higher cognitive functions, including language, are lateralized in cerebral cortex.

Neuropsychological studies on patients with brain lesions and rapid developments in brain imaging techniques have provided us with an increasing body of data on the functional aspects of language lateralization, but little is known about the substrate on which these specializations are realized.

Much attention has been focused on the gross size and shape of cortical regions involved, but recent findings indicate that the columnar and connectional structure within auditory and language cortex in the left hemisphere are distinct from those in homotopic regions in the right hemisphere.

These findings concern parameters that are closely linked to the processing architecture within the respective regions. Thus, the comparison of these microanatomical specializations with their respective functional counterparts provides important insights into the functional role of cerebral cortical organization and its consequences for processing of cortical information in the implementation of complex cognitive functions.
 


NOVEL NEW BRAIN IMAGING TECHNIQUE PINPOINTS AREAS
OF BRAIN MOST CRUCIAL FOR NORMAL FUNCTIONING


University of California, San Diego
April 21, 2003

A team of researchers led by cognitive scientist Elizabeth Bates, a professor at the University of California, San Diego, has developed a novel new brain imaging technique that produces maps that “light up” the relationship between the severity of a behavioral deficit and the voxels (similar to pixels in computer images) in the brain that contribute the most to that deficit.

Discovery of the new technique, known as Voxel-based Lesion-Symptom Mapping (VLSM), was reported in the April 21 issue of Nature Neuroscience. According to Bates, who is known for her research on the brain and how it is organized to process language, VLSM will give researchers an invaluable new tool for pinpointing the specific areas of the brain that are most crucial for normal functioning during critical brain activities, starting with the measures of language comprehension and production that were used for the first demonstration in Nature Neuroscience, but moving on to many different language and non-language functions. To view or download the paper, which includes color VLSM brain maps, please visit:
http://www.nature.com/cgi-taf/dynapage.taf?file=/neuro/journal/vaop/ncurrent/index.html

“This is a new brain mapping technique to be used with structural rather than functional magnetic resonance imaging scans (fMRI) that locate brain damage for individual patients,” said Bates. “It is an important breakthrough because it is a bridge, a tool, to bring two completely different traditions in brain research – lesion-behavior mapping and fMRI’s -- into alignment.”

Lesion-behavior mapping is the oldest technique in neuroscience, going back literally thousands of years. But, despite its many contributions, lesion analysis has not allowed researchers to examine functional networks in the brain. With functional brain imaging, the newest tool in cognitive neuroscience, researchers can identify the parts of the brain that are engaged when a patient undertakes such critical tasks such as language
comprehension, speech, or music perception. However, up until now, says Bates, these two techniques were not used together because there was no direct and quantifiable method for comparing them.

The VLSM method applied in this study represents an approach to lesion-symptom matching which uses voxel-based procedures inspired by those used in the analysis of functional neuroimaging data, avoiding some of the limitations of traditional lesion analysis methods. It is an improvement on previous lesion-symptom mapping techniques because it does not require patients to be grouped either by lesion site or behavioral cutoff, but instead exploits continuous behavioral and lesion information.

“The differences between lesion-symptom mapping (what brain areas are crucial for a behavior to be carried out) and activation in normal brains (what brain areas are merely along for the ride when a behavior is carried out) are just as important and informative as the similarities. Now we are in a position to conduct those comparisons,” said Bates.

In their study, the researchers applied VLSM to a group of 101 left-hemisphere damaged aphasic patients, using behavioral data from two well-studied tasks: language fluency and language comprehension. The VLSM maps for these variables confirm the anticipated contrast between anterior and posterior areas of the brain, while at the same time implicating interacting regions that also facilitate fluency and auditory comprehension and converge on new findings from modern brain imaging.

The VLSM technique is designed to match fMRI studies of the same behavioral functions in normal brains, which light up degrees of metabolic activity (by measuring blood flow) at different sites on a voxel-by-voxel basis. VLSM, which produces comparable pictures of the brain, shows the extent to which brain damage occupies each voxel. The researchers did a comparison of these patients that more accurately conveys how important each particular voxel is for the behaviour being measured.

“Put all those color-coded importance-level voxels together and you get lovely graded maps of degree-of-importance brain tissue for the behavior in question, maps that can be compared directly and quantitatively with the degree-of -activation maps that come out of functional brain imaging,” explained Bates.

It has taken Bates and her team 3-4 years to develop and refine the VLSM technique. She is in the process of sharing the VLSM software with other researchers and plans to make it available through the Internet, at no cost. Researchers involved in the study, which was funded by the National Institute on Deafness and Communication Disorders, include: Martin Sereno, Ayse Pinar Saygin, and Frederic Dick, UCSD Cognitive Science Department; Stephen Wilson, UCLA; Nina Dronkers, VA Northern California Health Care System and UC Davis; and Robert Knight, VA Northern California Health Care System and UC Berkeley.

Future work, said Bates, will focus on quantitatively comparing VLSM maps with activation maps from functional imaging studies of normal subjects performing the same of similar tasks.

Bates, a professor in UCSD’s Department of Cognitive Science in the Division of Social Sciences, is the director of the Center for Research in Language. Much of her work is interdisciplinary, involving large teams of neurologists, pediatricians, linguists, psychologists, computer scientist, and cognitive scientists.




The PDD Behavior Inventory: a rating scale for assessing response to intervention in children with pervasive developmental disorder

J Autism Dev Disord 2003 Feb;33(1):31-45

Cohen IL, Schmidt-Lackner S, Romanczyk R, Sudhalter V.
Department of Psychology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY

The PDD Behavior Inventory (PDDBI) is a rating scale filled out by caregivers or teachers that was designed to assess children having a Pervasive Developmental Disorder (PDD; autism, Asperger disorder, PDD-NOS, or childhood disintegrative disorder).

Both adaptive and maladaptive behaviors are assessed in the scale, making it useful for treatment studies in which decreases in maladaptive behaviors and improvements in adaptive social and language skills relevant to PDD are expected.

The adaptive behaviors assessed include core features of the disorder such as joint attention skills, pretend play, and referential gesture. The maladaptive behaviors sample a wide variety of behaviors observed in both lower- and higher-functioning individuals and include stereotyped behaviors, fears, aggression, social interaction deficits, and aberrant language.

The inventory was found to have a high degree of internal consistency. Inter-rater reliability was better for adaptive behaviors than for maladaptive behaviors. Factor analyses confirmed the structure of the PDDBI and indicated good construct validity.

In a subsample of children between 3 and 6 years of age, raw scores for adaptive behaviors increased with age in the parent and teacher versions, as did measures of social pragmatic problems. It was concluded that the PDDBI is both reliable and valid and is useful in providing information not typically available in most instruments used to assess children with PDD.





NEUROTRANSMITTER NEWS




Presynaptic control of quantal size: kinetic mechanisms and implications for synaptic transmission and plasticity

Guosong Liu
Current Opinion in Neurobiology, 2003, 13:3:324-331

Abstract

Although the strength of quantal synaptic transmission is jointly controlled by pre- and post-synaptic mechanisms, the presynaptic mechanisms remain substantially less well characterized. Recent studies reveal that a single package of neurotransmitter is generally insufficient to activate all available postsynaptic receptors, whereas the sum of transmitter from multiple vesicles can result in receptor saturation. Thus, depending upon the number of vesicles released, a given synaptic pathway might be either 'reliable' or 'unreliable'. A lack of receptor saturation in turn makes it possible to modify quantal size by altering the flux of transmitter through the synaptic cleft. Studies are now illuminating several new mechanisms behind the regulation of this transmitter flux — characteristics that control how transmitter is loaded into vesicles, how it is released and the manner by which it interacts with postsynaptic receptors.




Effects of chronic dizocilpine on acute pain and on mRNA expression of neuropeptides and the dopamine and glutamate receptors

Hassen A. Al-Amin, , a, Nayef E. Saadéb, Munir Khania, Samir Atwehc and Mohamed Jaberd

Department of Psychiatry, American University of Beirut Medical Center,
Department of Human Morphology and Physiology,
Department of Internal Medicine,
University of Poitiers, Poitiers, France

6 May 2003. 

Abstract

The mesocorticolimbic circuitry has been implicated in the pathophysiology of several neuropsychiatric syndromes like chronic pain and addiction.

The aim of this study was to evaluate the effects of dizocilpine (MK-801), a non-competitive N-methyl--aspartate (NMDA) receptor antagonist, on sensorimotor behaviors and the consequent changes in the dopamine, glutamate, and opiate systems in rats.

Five groups of rats were subjected to acute tests for nociception (hot plate and paw pressure) before and after MK-801 (0.05, 0.1, 0.2 and 0.4 mg/kg, i.p.) or saline. Another two groups received daily i.p. saline or MK-801 (0.4 mg/kg) for 15 days.

The nociceptive tests were performed on days 1, 7, and 14. On day 15 the rats received the last injection and were immediately sacrificed. We measured the mRNA expression, by in situ hybridization (ISH), of various dopamine and glutamate receptors, and enkephalin (Enk), dynorphin (Dyn), and substance P (SP) in the striatum, nucleus accumbens (NAC), piriform and cingulate cortex. Acute MK-801, dose-dependently, resulted in hyperalgesia.

The chronic effects of 0.4 mg/kg MK-801 showed an extinction of the acute hyperalgesic effects especially with the hot plate test. The ISH studies revealed a decrease in mRNA expression of Enk and SP in the striatum and NAC.

Our results indicate that the reversal of acute MK-801-induced hyperalgesia, with repeated exposure to systemic MK-801, is not directly related to changes in dopamine and glutamate receptors and might involve alteration of the striatal neuropeptide system.



Membrane and synaptic effects of corticotropin-releasing factor on periaqueductal gray neurons of the rat

Laura K. Bowers, Christa B. Swisher and Michael M. Behbehani
\
Brain Research, 2003, 981:1-2:52-57

Abstract

Corticotropin-releasing factor (CRF) has been identified as a major component of the hypothalamic–pituitary–adrenal (HPA) axis.

By stimulating the release of adrenocorticotropin hormone (ACTH), CRF acts as a key mediator of the stress response. However, CRF receptors and neuronal elements are present in many extrahypothalamic regions of the brain.

A region that contains both CRF-ergic neurons and CRF receptors is the midbrain periaqueductal gray (PAG). The physiological effects of CRF in the PAG are unknown.

In this study, an in vitro preparation, extracellular and intracellular patch-clamp recordings, were used to examine the effects of CRF, applied through an injecting electrode, on PAG neurons. Recordings were made from 147 neurons in the PAG. CRF injecting electrode concentrations of 0.05 and 1 µM were tested. At the higher concentration, CRF had a predominant excitatory effect on the neurons, and at the lower concentration, CRF produced no significant effect on the neurons.

The excitatory effect was dose dependent and was often associated with a depolarization in membrane potential in intracellular recordings. Application of the CRF antagonist, -helical CRF, blocked this excitatory effect.

It is concluded that CRF has a predominant excitatory effect on PAG neurons. It is also concluded that CRF is not acting presynaptically. This excitatory effect of CRF on PAG neurons may lead to activation of a descending analgesic pathway.



Protective autoimmunity against the enemy within: fighting glutamate toxicity

Michal Schwartz, Iftach Shaked, Jasmin Fisher, Tal Mizrahi and Hadas Schori
Trends in Neurosciences, 2003, 26:6:297-302

Abstract

Glutamate, a key neurotransmitter, is pivotal to CNS function. Alterations in its concentration can be dangerous, as seen for example in acute injuries of the CNS, chronic neurodegenerative disorders and mental disorders. Its homeostasis is attributed to the efficient removal of glutamate from the extracellular milieu by reuptake via local transport mechanisms.

Our recent studies suggest that glutamate, either directly or indirectly, elicits a purposeful systemic T-cell-mediated immune response directed against immunodominant self-antigens that reside at the site of glutamate-induced damage.

We suggest that the harnessed autoimmunity (which we have termed 'protective autoimmunity') helps the resident microglia in their dual function as antigen-presenting cells (serving the immune system) and as cells that clear the damaged site of potentially harmful material (serving the nervous system).

The interplay between glutamate and an adaptive immune response illustrates the bidirectional dialog between the immune and nervous systems, under both physiological and pathological conditions.

These results point to the possible development of a therapeutic vaccination with self-antigens, or with antigens cross-reactive with self-antigens, as a way to augment autoimmunity without inducing an autoimmune disease, thus providing a safe method of limiting degeneration.

This approach, which boosts a physiological mechanism for the regulation of glutamate, and possibly also that of other self-compounds, might prove to be a feasible strategy for therapeutic protection against glutamate-associated neurodegenerative or mental disorders.
 




AUTISM

Study suggests autistic children either don't absorb or don't excrete mercury

A study of mercury levels in the baby hair of children who were later diagnosed with autism has produced startling results.

The babies had far lower levels of mercury in their hair than other infants, leading to speculation that autistic children either do not absorb mercury or, more likely, cannot excrete it.

The results will be seized upon by parents who blame vaccines containing the mercury-based preservative thimerosal for their children's autism, some of whom are suing health authorities in the U.S. and Canada, according to a report in the June 21, 2003, New Scientist. (The measles-mumps-rubella [MMR] vaccine that some accuse of triggering autism, despite a lack of credible evidence, does not contain mercury.)

But while the study's findings support the theory that some children have a genetic fault that makes them far more susceptible to mercury poisoning, the results certainly do not prove this, or that thimerosal is involved. The difference in mercury levels in hair may be a sign of a more general problem in dealing with metals or it could simply be an anomaly that reveals little about what is happening elsewhere in the body, researchers say.

But if the results are confirmed, the conclusions of studies looking at the safety of low levels of mercury could also be called into question, says New Scientist (www.newscientist.com). Many of these studies relied on mercury levels in hair as a measure of exposure.

Autism experts say the findings are intriguing, but all emphasize the need for further studies. Although the findings are to be published in a peer-reviewed journal, some critics say the results are rather too striking, and point out that the researchers who did the work all believe that thimerosal is to blame for autism.

The team leader, Louisiana doctor Amy Holmes, in fact set out to try to prove that autistic children had been exposed to high levels of mercury. She obtained baby hair from parents who had kept the first cuttings and sent off a few samples for analysis. To her surprise, mercury levels were low.

Holmes has now done a bigger study, comparing mercury levels in first baby haircuts from 94 autistic children with those of 45 other children. The mean level in the baby hair of children later diagnosed as autistic was 0.47 parts per million, compared with 3.63 ppm in the others, the team found - nearly a tenth lower. What's more, the more severe the autism, the lower the mercury levels. The mean levels of children with mild, moderate, and severe autism were 0.79, 0.46, and 0.21 ppm, respectively.

Most of this mercury came from the mothers. The main sources of exposure, according to the team, were mercury amalgam fillings, Rho D immunoglobulin injections containing thimerosal given to Rhesus negative mothers, and heavy consumption of fish (defined as more than five fish meals a month). In the control group, hair mercury rose in line with the mothers' exposure. But the baby hair of autistic children had consistently low mercury levels, even when the mothers' exposure was high, the team found.

The results are scheduled for publication in the International Journal of Toxicology in September 2003.

One explanation, says team member Mark Blaxill of the campaign group SafeMinds of Cambridge, Massachusetts, is a problem with metal uptake. If so, autistic children might also be deficient in metals essential for brain development such as zinc, iron, and copper. Alternatively, some children may have a problem excreting mercury. The metal might then build up in the brain, producing autism. Most mercury is excreted in urine and feces, but the lack of mercury in hair might be a sign that the metal is being retained in cells rather than getting into the blood, the researchers suggest.

Mercury is one of the suspected causes of autism, with proponents arguing that there many similarities between autism and mercury poisoning. But a review published earlier in 2003 pointed out that poisoning by the different forms of mercury found in fish, fillings, and thimerosal has effects distinct from autism, and concluded that what little evidence there is does not support any link.

Despite this, some doctors, including Holmes, have been experimenting with giving autistic children metal-binding agents, or chelators, to rid the body of heavy metals.

"They are loaded to the gills with metals," Holmes, who was unavailable for comment, claimed last year. The only published evidence, however, is a very small study from 1976 suggesting autistic children have higher levels of lead in their blood.

Critics such as child neurologist Emanuel Dicicco-Bloom of the Robert Wood Johnson Medical School in New Jersey says concluding that autistic children accumulate mercury on the basis of low levels in hair is a big logical leap that is not justified by the evidence. Even some of those who blame heavy metals such as mercury for autism echo his warnings not to try potentially dangerous therapies such as chelation. Parents should wait for the results of the clinical trials about to begin, they say.

And Dicicco-Bloom's colleague Mike Gochfield, who does mercury testing, says that the levels of mercury in the control group are way above what he would expect for children in the U.S.

Blaxill's response is that no one has ever tested first baby haircuts before, so there are no "normal" results to compare to. The lab that did the testing was not told which children the samples were from, he adds.

And according to unpublished work by Steve Lindow and Steve Haslow at the University of Hull in the U.K., reported New Scientist, hair mercury levels in newborns can be even higher than in the mother. They suspect that mothers may actively transport metals to the fetus. But on average the first baby hair in Holmes' study was cut at 18 months old, so this would not explain the high levels in the controls.

Astonishingly, only one other published study, from 1985, has compared mercury levels in the hair of children with and without autism. That study found no difference, but it did find lower levels of metals such as calcium, copper, and chromium - levels that were so distinctive they could be used as a "diagnostic tool for autism," the report said.

Other experts say the theory that autistic children are particularly at risk from heavy metals is at least plausible.

"This kind of gene-environment interaction is not incompatible with the known heritability of autism," says Simon Baron-Cohen of Cambridge University. "If these results hold up, metal studies on the brain could be revealing." This article was prepared by Health & Medicine Week editors from staff and other reports.






EEG/ERP

Disruption of early event-related theta synchronization of human EEG in alexithymics viewing affective pictures

Neurosci Lett 2003 Apr 3;340(1):57-60

Aftanas LI, Varlamov AA, Reva NV, Pavlov SV.
Psychophysiology Laboratory, State Research Institute of Physiology, Siberian Branch, Russian Academy of Medical Sciences, Novosibirsk, Russia

The 62-channel EEG was recorded while control non-alexithymic (n=21) and alexithymic (n=20) participants viewed sequentially presented neutral, pleasant and unpleasant pictures and subjectively rated them after each presentation.

The event-related synchronization (ERS) to these stimuli was assessed in the theta-1 (4-6 Hz) and theta-2 (6-8 Hz) frequency bands. The obtained findings indicate that alexithymia influences perception of only emotional stimuli. Over anterior cortical regions alexithymia vs. control individuals in response to both pleasant and unpleasant stimuli manifested decreased left hemisphere ERS in the early test period of 0-200 ms along with enhanced ERS in response to negative vs. positive and neutral stimuli in the right hemisphere at 200-600 ms after stimulus onset.

The findings provide the first EEG evidence that alexithymia construct, associated with a cognitive deficit in initial evaluation of emotion, is indexed by disrupted early frontal synchronization in the upper theta band that can be best interpreted to reflect disregulation during appraisal of emotional stimuli.

BRAIN INJURY NEWS

Development of a longitudinal study of complications and functional outcomes after traumatic brain injury

Brain Inj 2003 Apr;17(4):265-78

Labi ML, Brentjens M, Lou Coad M, Flynn WJ, Zielezny M.
State University of New York at Buffalo, School of Medicine and Biological Sciences, Buffalo, NY, USA.

Primary objective: To create a longitudinal database of patients with moderate and severe traumatic brain injury.

Research design: A prospective study design was used to collect data pertaining to demographics, acute and post-acute management, complications, resource utilization and functional outcomes.

Methods and procedures: Data were collected on 233 patients with a Glasgow Coma Score of 12 or less, admitted to a Level 1 Trauma Centre within 24 hours of injury and continued through post-hospitalization follow-up.

Main outcomes and results: The mean age was 37.7 years, 70% were males, 54% were motor vehicle related accidents, and 21% died. Of the 185 survivors, 23% were discharged directly home from acute hospital care and 74% required inpatient rehabilitation. At hospital discharge, 76% had Rancho Los Amigos Scores of VII or higher; 81% had no or only mild verbal communication deficits and 79% were able to ambulate.

Conclusions: The study indicates that while it is difficult to predict functional outcomes for individual survivors of TBI in the early stages of acute care, they are often better than suspected at the time of injury.






ADD/ADHD

Association of ADHD and conduct disorder--brain electrical evidence for the existence of a distinct subtype

J Child Psychol Psychiatry 2003 Mar;44(3):356-76

Banaschewski T, Brandeis D, Heinrich H, Albrecht B, Brunner E, Rothenberger A.
Child and Adolescent Psychiatry, University of Gottingen, Germany.

BACKGROUND: To evaluate the impact of psychopathological comorbidity with oppositional defiant/conduct disorder (ODD/CD) on brain electrical correlates in children with attention deficit hyperactivity disorder (ADHD) and to study the pathophysiological background of comorbidity of ADHD+ODD/CD.

METHOD: Event-related potentials (ERPs) were recorded during a cued continuous performance test (CPT-A-X) in children (aged 8 to 14 years) with ICD-10 diagnoses of either hyperkinetic disorder (HD; n = 15), hyperkinetic conduct disorder (HCD; n = 16), or ODD/CD (n = 15) and normal children (n = 18). HD/HCD diagnoses in all children were fully concordant with the DSM-IV diagnosis of ADHD-combined type.

ERP-microstates, i.e., time segments with stable brain electrical map topography were identified by adaptive segmentation. Their characteristic parameters and behavioral measures were further analyzed.

RESULTS: Children with HD but not comorbid children showed slower and more variable reaction times compared to control children. Children with HD and ODD/CD-only but not comorbid children displayed reduced P3a amplitudes to cues and certain distractors (distractor-X) linked to attentional orienting.

Correspondingly, global field power of the cue-CNV microstate related to anticipation and preparation was reduced in HD but not in HCD. Topographical alterations of the HD occurred already in the cue-P2/N2 microstate.

In sum, the comorbid group was less deviant than both the HD-group and the ODD/CD-group.

CONCLUSIONS: The findings suggest that HD children (ADHD-combined type without ODD/CD) suffer from a more general deficit (e.g., suboptimal energetical state regulation) including deficits of attentional orienting and response preparation than just a responseinhibitory deficit, backing the hypothesis of an involvement of a dysregulation of the central noradrenergic networks.

The results contradict the hypothesis that ADHD+ODD/CD represents an additive co-occurrence of ADHD and ODD/CD and strongly suggest that it represents a separate pathological entity as considered in the ICD-10 classification system, which differs from both HD and ODD/CD-only.



NEURO-PROCESSING NEWS

Brain links pain with pleasure
New treatments for pain could be developed

Massachusetts General Hospital


Scientists have found that areas of the brain that respond to feelings of pleasure also react to the sensation of pain.

The findings could lead to a better understanding of the effects of pain within the brain and to new ways to diagnose and treat pain.

The new research carried out by the USA's Massachusetts General Hospital (MGH) backs up previous studies.

Understanding this emotional component would be key to developing new approaches to helping chronic pain

Dr David BorsookThe MGH's Dr David Borsook said: "Pain is a complex experience that includes both a sensation and an emotional reaction.

"Understanding this emotional component would be key to developing new approaches to helping chronic pain in patients, who are at increased risk for anxiety, depression and suicide."

Researchers used a technique called functional magnetic resonance imaging (fMRI) to take pictures of the brains of eight study volunteers.

The eight young men had a thermode or small heat pad attached to their hands, which administered warm or hot temperatures for brief periods, alternating with normal skin temperatures.

Brain images focused both on areas previously identified as being involved with the sensory experience of pain and on those found in earlier studies to be activated by response to such stimuli as cocaine, food and money.

Objective pain tests

The results showed the painful "hot" temperatures caused activation not only of the classic pain circuitry in the brain, but also some of the areas previously described as reward circuitry.

The reward circuits responded more quickly than the pain circuits during the administration of hot temperatures.

The pain circuits were active towards the end of the heat administration period.

Lino Becerra, one of the authors of the study, said: "These are two systems that were never associated in the past and it's the first time we have seen something aversive activating these reward structures."

Co-author Dr Hans Breiter said: "It would appear the philosophers Spinoza and Bentham, who proposed that pleasure and pain were part of the same spectrum, were right."


Tests activated pleasure and pain circuits

The scientists go on to suggest this response is due to circuits in the brain that handle reward trying to analyse stimuli and judge which are important to survival.

It is hoped these conclusions could pave the way for developing objective tests to measure pain and pain relief and the creation of pain-relieving drugs that target the structures previously associated with reward.

This strategy could lead to the treatment of pain that does not respond to traditional medications.

British pain imaging expert Dr Irene Tracey from Oxford University believes such findings could bring hope of developing alternative pain remedies, which do not involve drugs.

She said: "This research provides information which is critical for future studies that will pave the way for pain sufferers being given alternative therapies to combat their suffering."





Neuropsychiatric applications of transcranial magnetic stimulation: a meta analysis

The International Journal of Neuropsychopharmacology (2002), 5:73-103 Cambridge University Press
Copyright © 2002 Collegium Internationale Neuropsychopharmacologicum
Tal Burt , Sarah H. Lisanby and Harold A. Sackeim
Department of Biological Psychiatry, New York State Psychiatric Institute, New York, USA
Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY, USA
Radiology, College of Physicians and Surgeons of Columbia University, New York, NY, USA


Transcranial magnetic stimulation (TMS) is a technology that allows for non-invasive modulation of the excitability and function of discrete brain cortical areas.

TMS uses alternating magnetic fields to induce electric currents in cortical tissue. In psychiatry, TMS has been studied primarily as a potential treatment for major depression. Most studies indicate that slow-frequency repetitive TMS (rTMS) and higher frequency rTMS have antidepressant properties.

A meta-analysis of controlled studies indicates that this effect is fairly robust from a statistical viewpoint. However, effect sizes are heterogeneous, and few studies have shown that rTMS results in substantial rates of clinical response or remission, and the durability of antidepressant effects is largely unknown.

We review in detail rTMS studies in the treatment of depression, as well as summarize treatment studies of mania, obsessive–compulsive disorder, post-traumatic stress disorder, and schizophrenia. We also review the application of TMS in the study of the pathophysiology of psychiatric disorders and summarize studies of the safety of TMS in human subjects.

DEPRESSION


Concussions, Depression May Be Linked

By LAURAN NEERGAARD, AP Medical Writer

WASHINGTON - Retired football players who suffered three or four concussions have twice the risk of later developing clinical depression — a risk that rises with even more injuries, new research says.

It's the latest finding that suggests what many people consider merely a bang really can have long-term repercussions. Now scientists are beginning intensive imaging studies to pin down just what happens inside the brain when someone suffers a concussion.


It's not a concern only for professional athletes. Concussions, a mild brain injury, can be caused by any hard blow or jolt to the head — from whiplash during a car accident to a tumble onto a sidewalk. An estimated 1.1 million Americans suffer a concussion each year.


But athletes, both professional and amateur, are more likely than the average person to suffer repeated concussions.


That's a particular problem because concussions can be hard to diagnose — and if you get banged around again before you've fully healed and you can suffer potentially deadly brain swelling. Still, specialists say athletes often beg to get back in the game, swearing they're fine.


"I always say, 'You can ice your ankle but you can't ice your brain,'" says Dr. Julian Bailes of West Virginia University's School of Medicine. "You don't send a player who's still symptomatic back to play."


Most people fully recover from a concussion. But a fraction suffer lingering, sometimes severe, problems with memory and other functions — and doctors wonder if sufferers of bad or repeated concussions are more prone to neurologic disease later in life.


As a first step in studying that question, Bailes and colleagues from the University of North Carolina's Center for the Study of Retired Athletes analyzed data from almost 2,500 retired National Football League players.

Bailes found no link between concussions and later Alzheimer's disease or strokes, two common worries.


But 263 of the retired players suffered depression. Having three or four concussions meant twice the risk of depression as never-concussed players — and five or more concussions meant a nearly threefold risk.


The study, presented last week at an American Association of Neurological Surgeons meeting, supports earlier research that linked concussions suffered by World War II soldiers to depression decades later.


For better proof, University of Pittsburgh neuropsychologist Mark Lovell now is tracking how NFL and National Hockey League players fare in the years after a concussion.


More intriguing, he's using advanced MRI scanners to image the brains of high school athletes in a study that will rescan up to 250 of them who go on to suffer a concussion — providing before-and-after shots that could finally show just what the injury does to delicate brain tissue.


Scientists already know a concussion somehow throws crucial brain-chemical reactions out of whack, but they're not sure for how long — key to deciding when the patient is healed — or if that imbalance could cause a chain reaction leading to later problems like depression.


For now, Lovell and other specialists want athletes and their coaches and relatives to start taking concussions more seriously.


"If you get hit and have a headache, don't do the macho routine — you need tell somebody," Lovell says.


Look hard for symptoms — they're not always obvious in an adrenaline-pumped athlete. Loss of consciousness, from a few seconds to a half-hour, is the best-known symptom but doesn't always occur. Other symptoms include confusion, persistent headache, cognitive problems, fatigue and changes in mood, vision or hearing.

Particularly crucial is short-term memory: How long before you were hit can you remember? The longer the period of amnesia, the worse the concussion.

Watch for changes in behavior, signs that signal pain the patient denies.

Coaches have long thought that if obvious symptoms disappear within 15 minutes, it's safe to put a player back in the game. But last winter, Lovell discovered that teenage athletes with the mildest of concussions often have subtle memory and other symptoms days later — refuting that advice.

Rest is the only way to heal, and Lovell's research suggests that takes about a week.

How many concussions is too many? Each one suffered seems to render someone more vulnerable to another, but "there's no magic number that we know at this point in time where you can say, 'OK, you've now had that final one concussion too many,'" Lovell says.



AUDITORY NEWS

Hemispheric asymmetries in cerebral cortical networks

Jeffrey Hutsler and Ralf A.W. Galuske
Trends in Neurosciences, (July 07, 2003), 10.1016/S0166-2236(03)00198-

Abstract

Since the middle of the 19th century it has been recognized that several higher cognitive functions, including language, are lateralized in cerebral cortex.

Neuropsychological studies on patients with brain lesions and rapid developments in brain imaging techniques have provided us with an increasing body of data on the functional aspects of language lateralization, but little is known about the substrate on which these specializations are realized.

Much attention has been focused on the gross size and shape of cortical regions involved, but recent findings indicate that the columnar and connectional structure within auditory and language cortex in the left hemisphere are distinct from those in homotopic regions in the right hemisphere.

These findings concern parameters that are closely linked to the processing architecture within the respective regions. Thus, the comparison of these microanatomical specializations with their respective functional counterparts provides important insights into the functional role of cerebral cortical organization and its consequences for processing of cortical information in the implementation of complex cognitive functions.

SPEECH AND LANUGAGE

Emergent constraints on word-learning: a computational perspective

Terry Regier
Trends in Cognitive Sciences, 2003, 7:6:263-268

Abstract

In learning the meanings of words, children are guided by a set of constraints that give privilege to some potential meanings over others. These word-learning constraints are sometimes viewed as part of a specifically linguistic endowment. However, several recent computational models suggest concretely how word-learning – constraints included – might emerge from more general aspects of cognition, such as associative learning, attention and rational inference. This article reviews these models, highlighting the link between general cognitive forces and the word-learning they subserve. Ultimately, these cognitive forces might leave their mark not just on language learning, but also on language itself: in constraining the space of possible meanings, they place limits on cross-linguistic semantic variation.




Linguistic differences and language design

Mark C. Baker

Trends in Cognitive Sciences, (July 16, 2003), 10.1016/S1364-6613(03)00157-8

Abstract

A small number of discrete choices ('parameters') embedded within a system of otherwise universal principles create the extensive superficial differences between unrelated languages like English, Japanese, and Mohawk.

Most current thinking about the evolution of language ignores or denies the existence of these parameters because it can see no rationale for them. That the human language faculty is organized in this way makes more sense if language is compared to a cipher or code. As such, it would have a purpose of concealing information from some at the same time as it communicates information to others.




Language evolution: consensus and controversies

Trends in Cognitive Sciences, 2003, 7:7:300-307

Abstract

Why is language the way it is? How did language come to be this way? And why is our species alone in having complex language? These are old unsolved questions that have seen a renaissance in the dramatic recent growth in research being published on the origins and evolution of human language.

This review provides a broad overview of some of the important current work in this area. We highlight new methodologies (such as computational modeling), emerging points of consensus (such as the importance of pre-adaptation), and the major remaining controversies (such as gestural origins of language).

We also discuss why language evolution is such a difficult problem, and suggest probable directions research may take in the near future.

VISION/VISUALIZATION

Strange vision: ganglion cells as circadian photoreceptors

David M. Berson

Trends in Neurosciences

A novel photoreceptor of the mammalian retina has recently been discovered and characterized. The novel cells differ radically from the classical rod and cone photoreceptors. They use a unique photopigment, most probably melanopsin. They have lower sensitivity and spatiotemporal resolution than rods or cones and they seem specialized to encode ambient light intensity. Most surprisingly, they are ganglion cells and, thus, communicate directly with the brain. These intrinsically photosensitive retinal ganglion cells (ipRGCs) help to synchronize circadian rhythms with the solar day. They also contribute to the pupillary light reflex and other behavioral and physiological responses to environmental illumination.




The visual word form area: expertise for reading in the fusiform gyrus

Bruce D. McCandliss, Laurent Cohen and Stanislas Dehaene
Trends in Cognitive Sciences, 2003, 7:7:293-299

Abstract

Brain imaging studies reliably localize a region of visual cortex that is especially responsive to visual words. This brain specialization is essential to rapid reading ability because it enhances perception of words by becoming specifically tuned to recurring properties of a writing system. The origin of this specialization poses a challenge for evolutionary accounts involving innate mechanisms for functional brain organization. We propose an alternative account, based on studies of other forms of visual expertise (i.e. bird and car experts) that lead to functional reorganization. We argue that the interplay between the unique demands of word reading and the structural constraints of the visual system lead to the emergence of the Visual Word Form Area.
   

OBSESSIVE COMPULSIVE DISORDER

A preliminary morphometric magnetic resonance imaging study of regional brain volumes in body dysmorphic disorder.

Psychiatry Res 2003 Jan 20;122(1):13-9

Rauch SL, Phillips KA, Segal E, Makris N, Shin LM, Whalen PJ, Jenike MA, Caviness VS, Jr, Kennedy DN.
Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School,

Morphometric magnetic resonance imaging (MRI) was used to compare regional brain volumes in eight women with body dysmorphic disorder (BDD) and eight healthy comparison subjects. The BDD group exhibited a relative leftward shift in caudate asymmetry and greater total white matter vs. the comparison group. Findings with respect to the caudate nucleus are consistent with both the conceptualization of BDD as an obsessive-compulsive spectrum disorder, and the 'striatal topography model' of obsessive-compulsive disorders.




MEMORY



A role for inhibition in shaping the temporal flow of information in prefrontal cortex

Christos Constantinidis, Graham V. Williams & Patricia S. Goldman-Rakic
Department of Neurobiology, Yale University School of Medicine

The prefrontal cortex is important in guiding or inhibiting future responses, which requires the temporal integration of events and which provides continuity to the thought process. No cellular mechanism has been proposed to explain how the mental representation of a response or idea is linked to the next. Using simultaneous recordings in monkeys, we revealed inhibitory interactions between neurons active at different time points relative to the cue presentation, delay interval and response period of a working memory task. These findings suggest an important role of inhibition in the cerebral cortex—controlling the timing of neuronal activities during cognitive operations and thereby shaping the temporal flow of information.






Human recognition memory: a cognitive neuroscience perspective

Michael D. Rugg and Andrew P. Yonelinas
Trends in Cognitive Sciences, 2003, 7:7:313-319

Abstract

For many years the cognitive processes underlying recognition memory have been the subject of considerable interest in experimental psychology. To account for a broad range of behavioral findings, psychologists have put forward a variety of 'dual-process' models, all of which propose that recognition memory is supported by two forms of memory – familiarity and recollection – that differ in their speed of operation and the specificity of the retrieved information.

More recently, the dual-process framework has been extended to encompass findings from studies investigating the neural basis of recognition memory. Results from neuropsychological, ERP and functional neuroimaging studies can be accommodated within the framework, and suggest that familiarity and recollection are supported by distinct neural mechanisms.
 



Changes in behavior-related neuronal activity in the striatum during learning

Trends in Neurosciences

Wolfram Schultz, Léon Tremblay and Jeffrey R. Hollerman

Abstract

The involvement of the striatum in numerous forms of learning and memory is likely to be based on changes in neuronal activity when specific behavioral tasks are being learned.

Striatal neurons show distinctive changes when animals learn the significance of stimuli that predict rewards and induce the preparation of movements. These changes resemble some of the simultaneous, learning-related changes in closely associated areas of the frontal cortex.

The striatal changes might assist in adapting existing reward expectations and behaviors to novel or changing environmental conditions and they could contribute to the functions of the basal ganglia in learning, reward expectation and movement preparation




NUTRITIONAL NEWS

Celiac disease (Wheat Intolerance) More Common

Celiac disease, an autoimmune disease of the gut, may be more common than previously thought, according to a study. The disease may affect as many as one in 99 children and is triggered when people who are genetically predisposed consume proteins found in wheat, barley and rye.

Children with severe celiac disease have trouble absorbing nutrients, which can lead to weight loss and anemia. Researchers have also discovered mild forms of the disease that have symptoms unrelated to the gut.

Further, adults may have the condition for many years without knowing because the symptoms vary widely, making the disease difficult to diagnose. Undiagnosed celiac disease can result in osteoporosis, chronic fatigue, anemia, miscarriages and behavioral changes, researchers noted.

In the United States, it took as many as 12 to 13 years after symptoms occurred for patients to be diagnosed with celiac disease, according to another study.

Celiac disease is treated with a gluten-free diet. Gluten is the protein that triggers the reaction.

In the study, examined the blood, which had been collected in 1994 for a previous study, from 3,654 students aged 7 to 16 years.

It was found that although 56 of the children tested positive for the disease, only 10 had been diagnosed with celiac disease as of 2001.

Researchers then did a biopsy of the intestines of 36 of the children who had tested positive to check against the blood test results. Of these children, 27 had signs of celiac disease according to the biopsy.

The diet used to treat celiac disease can be challenging as patients can't consume pasta, bread, cookies or beer, and gluten is often used in prepared foods but not listed on labels.

Researchers noted that people are more likely to stick with the diet if their symptoms resolve as a result.

New England Journal of Medicine June 19, 2003;348:2517-2524,2568-2570

DR. MERCOLA'S COMMENT: This is not new, and for that matter, is not even accurate information. However, it is a step in the right direction. For the longest time it was believed that celiac disease was a very rare condition only present in one in 5,000 people. However, even as long as three years ago I have posted studies that show that one in 33 people have celiac disease. That is 300 percent more prevalent than this NEJM study shows.

Most people don't realize that there are many reactions to wheat, aside from celiac disease, that can cause health problems. Most of us are addicted to breads, bagels, pizza, pasta, waffles and pancakes and would rather die than give them up, and many people do just that, die from the side effects of eating wheat.

Wheat, especially whole wheat, is not bad for everyone, just most people in this country. It is quite clear that if you are overweight you would best be served by avoiding wheat, even organic whole-wheat products, as they will contribute to elevated insulin levels that will disrupt your biochemistry and impair your ability to lose weight.

A recent book, Dangerous Grains, reviews this topic quite comprehensively, and, as many of you know, one of the key components of my nutrition plan is vastly reducing or eliminating the grains in your diet, as this will lead to optimum health.

My book, The No-Grain Diet, provides you with a comprehensive and practical approach to implementing an individualized dietary plan with the aid of Metabolic Typing. This will lead you to healing, achieving your ideal weight and attaining optimal health.

In addition to its focus on my nutrition plan, what sets The No-Grain Diet apart from other dietary and health books is my focus on maintaining the healthy habits you adopt; whether people change their diet to lose weight, heal a disease, guard against illness or simply improve their health, they are often successful at the start.

However, as time goes by, most will fall right back into the old patterns that sabotaged their health in the first place. This is because the focus was solely on changing negative physical habits, and not the negative emotions contributing to those habits. In The No-Grain Diet, I will show you how, by using EFT, you can eliminate those negative emotions--and maintain your healthy eating plan and lifestyle for good.

As for the gluten referenced in the article above, it is a protein in wheat, barley, rye, oats and spelt that can cause problems in many individuals who are completely independent of its disruption of insulin homeostasis.

As for grains in the human diet overall, there is fairly strong evidence that in Paleolithic times some 10,000 years ago most humans did not consume many grains; they were hunter-gatherers who subsisted mostly on vegetables and meats. But, 10,000 years is a mere blip in a biological sense for humans: over 99 percent of our genetic make-up was in place, in fact, before we ever started consuming grains.

When considered from this perspective alone, it is not too surprising that grains can cause a wide array of health issues. Contemporary humans have not suddenly evolved mechanisms to incorporate the high carbohydrates from starch- and sugar-rich foods into their diet.

Some of my patients ask me if grains are bad, why would the Bible reference them as acceptable? I am not a biblical scholar and so cannot comment on whether the words used in the Bible (and translated from original sources) actually mean "grains" or food in some larger sense.

Regardless, I am not making an absolute blanket statement that grains are bad; instead, I am stating that most of us would benefit by either drastically reducing or eliminating them from our diet.





Gluten-Free: New Diet for the 21st Century-Expert's Advice on Dealing With Ever-Increasing Food Choices

DENVER, Jul 29, 2003 /PRNewswire via COMTEX/ -- Move over, sugar-free and fat-free. Make room for gluten-free -- a new lifestyle that's revolutionizing the way we eat.

About 10-15% of Americans can't eat gluten, a protein in wheat and related grains, because -- although wheat is the all-American grain -- it can actually be toxic for some people, says Carol Fenster, Ph.D., author of Gluten-Free 101, a guide to the gluten-free lifestyle, available at www.glutenfree101.com.

"With the explosion in food choices -- 7000 supermarket products in the 1960's, according to the Institute of Food Technology, compared to 40,000 now," says Fenster, "today's consumers must sharpen their label-reading skills to detect hidden gluten in an overwhelming array of ready-made products. They also have to master restaurant dining and being a discerning, yet considerate guest in other people's homes."

Gluten-sensitivity takes many forms, says Fenster. It can be an auto-immune condition called celiac disease that inhibits nutrient absorption. Or it can be intolerances or food allergies. But regardless of the reason, living gluten-free means a new way of eating.

The lifestyle change that's perhaps hardest to make for some people -- yet the most rewarding -- is learning to prepare one's food at home, says Fenster whose own gluten intolerance is a catalyst for her six books that help others prepare gluten-free foods in their own kitchens.

"The things we miss the most on a gluten-free diet -- pizza, bread, bagels, and other baked goods -- are the hardest foods to find in stores, let alone restaurants," says Fenster. So she mastered the fail-proof, gluten-free versions and shares how to do it in her book -- along with lots of help and encouragement for the novice or kitchen-challenged cook. Her nationally-acclaimed pizza crust recipe is on her web site at www.glutenfree101.com, along with photos showing exactly how to prepare it.

"I'm a firm believer in the benefits of home cooking," says Fenster. "Food prepared at home gives you control over what's in it -- and how it's prepared. And, studies show that home-cooked food contains less fat, sugar, and calories." Plus, she adds, "freshly prepared food just tastes better."






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