Traumatic Brain Injury (TBI) is a condition that is well understood in its causes and the consequences to the physical brain itself, but, the implication of childhood TBI on the neurological development of the child, (particularly the development of cognitive and functional skills) is an area that requires much further investigation according to researchers from Australia (Melbourne, Victoria)(1).

Many parents, teachers and professionals dismiss the ramifications of an early childhood TBI in the later neurological development of a child. Childhood TBI is the most common cause of disrupted neurological development. Between 219 and 345 in a 100,000 children experience a TBI annually (2,3). 1 in 30 newborns will suffer a TBI by the age of 16 (2). Children under the age of three have double the risk of a TBI than any other age group throughout childhood (3). Children in this category suffer from a high proportion of falls which result in moderate to severe TBI. However, those who experience TBI as the result of motor vehicle crashes and pedestrian vehicular injuries suffer the most severe axonal injury due to acceleration and deceleration forces on the brain (4). There are three reasons for this:
1. A thin and pliable skull is at increased risk of diffused injury (5,6)
2. Increased susceptibility to neuronal shearing and rotational forces because the head is much larger than the body with weak neck muscles. (6,7)
3. Blood vessels are highly elastic(6)
This leads to more significant brain damage (mass lesion, subdural haemotoma, tears in the white matter of the frontal lobes) after TBI in children under the age of three than in older children.

It is a common misconception that the brain rewires itself after a TBI and that nothing is really affected some two, five or ten years later. This misconception is all the more alarming because 1 in 3 children who experience a TBI will endure permanent brain damage(2).

Researchers in Melbourne have found evidence that challenges this myth that young children are more resilient to TBI(1). Their longitudinal study selected patients from the Royal Melbourne Hospital during 1993 to 1997 and showed that young children who suffered a severe TBI before the age of three show lower intelligence (1-2 Standard Deviations lower than the mean IQ for their age) than their healthy counterparts ten years post injury (1). This suggests global and persisting intellectual deficits in children who have suffered a serious TBI in childhood.

Furthermore, a child’s preinjury social functioning and environmental factors such as socio-economic status (SES) were good predictors of their outcome in 10 years post injury(1). SES has been closely related to early TBI not only in its relationship with the recovery itself, but also as a causative factor of the initial TBI (3). In fact in injuries on children less than three years of age, the SES of the family is the strongest predictor of intellectual functioning, when the children were tested at four and six years old(13 as cited in 8). However, this study further illustrated that regardless of the severity of the TBI, recovery rate plateaus between five and ten years showing that there is no significant relationship between the rate of recovery and the severity of the injury (1).

Furthermore, preinjury adaptive function (social function) was predictive of 10 year adaptive abilities with social and behavioural outcomes being predicted by family function (1). Since children at this age are developing neurobehavioural skills, they have an increased risk of disrupted development and clinical reports suggest residual problems in cognition, attention, executive function and memory (9, 10). These children therefore may have difficulty or fail to acquire adaptive behaviors, academic skills and appropriate social behaviors and skills (11, 12). Other predictors of long-term behavioural, social and intellectual development of the individual who experiences an early childhood TBI include the parental mental health as well as family and parental function (8).

In addition to intellectual deficits, social deficits are also common after early childhood TBI. In another study, it was found that children who suffer from a TBI before the age of four experience greater difficulties socialising than their healthy counterparts (13).

These findings are inconsistent with the argument that young children grow into deficits throughout childhood (4,14,15) and instead appears to indicate a consistent lag in comparison to healthy children. Persistent intellectual impairment is more likely to arise from TBI involving high levels of acceleration and deceleration forces to the brain (motor vehicles, motor bikes and pedestrian automobile related injuries) which produce severe white matter injury that is diffuse or multi-focal.

The management of TBI is multimodal and involves diet and nutrition; motor coordination; memory retraining; neurofeedback and improving auditory processing skills. For more information on the management of TBI, please see the articles on Neurofeedback and TBI. For initial consultations and assessments, please contact the office during business hours to make an appointment on (02) 9637 9998.

References:
1. Anderson V, Godfrey C, Rosenfeld JV, Catroppa C. Predictors of Cognitive Function and Recovery 10 Years After Traumatic Brain Injury in Young Children. Pediatrics. 2012;129:254-261.
2. Kraus JF. Epidemiological features of brain injury in children, In: Broman SH, Michel ME, eds. Traumatic Head Injury in Children. New York, NY: Oxford University Press; 1995: 117 – 146.
3. Crowe L, Babl F, Anderson V, Catroppa C. The epidemiology of paediatric head injuries: data from a referral centre in Victoria, Australia. J Paediatric Child Health. 2009; 45(6); 346-350.
4. Levin HS. Long-term intellectual Outcome of Traumatic Brain Injury in Children: Limits to Neuroplasticity of the Young Brain? Pediatrics 2012;129(2):494-495.
5. Hanh YS, Chyung C, Barthel MJ, Bailes J, Flannery AM, McLone DG. Head Injuries in children under 36 months of age. Demography and outcome. Childs Nerv Syst. 1988;4(1): 34-40.
6. Case ME. Forensic Pathology of child brain trauma. Brain Pathol. 2008;18(4):562-564.
7.Margulies SS, Thibault KL. Infant Skull and suture properties: measurements and implications for mechanisms of pediatric brain injury. J Biomech Eng. 2000;122(4):364-371.
8. Crowe LM, Catroppa C, Babl FE, Anderson V. Intellectual, Behavioral and Social Outcomes of Accidental Traumatic Brain Injury in Early Childhood. Pediatrics2012;129(2):262-268.
9. Anderson V, Catroppa C, Morse S, Haritou F, Rosenfeld JV. Intellectual outcome from preschool traumatic brain injury: a 5-year prospective, longitudinal study. Pediatrics. 2009; 124(6).
10. Jaffe KM, Fay GC, Polissar NL, et al. Severity of pediatric traumatic brain injury and neurobehavioural recovery at one year–a cohort study. Arch Phys Med Rehabil. 1993;74(6):587-595.
11. Benz B, Ritz A, Kiesow S. Influence of age-related factors in long-term outcome after traumatic brain Injury (TBI) in children: a review of recent literatire and some preliminary findings. Restor Neurol Neurosci. 1999;14(2-3): 135-141.
12. McKinlay A, Dalrymple-Alford JC, Horwood LJ, Fergusson DM. Long term psychosocial outcomes after mild head injury in early childhood. J Neurol Neurosurg Psychiatry. 2002; 73(3):281-288.
13. Sonnerberg LK, Dupuis A, Rumney PG. Pre-school traumatic brain injury and its impact on social development at 8 years of age. Brain Inj. 2010;24(7-8):1003-1007.
14. Giza CC, Prins ML. Is being plastic fantastic? Mechanisms of altered plasticity after developmental traumatic brain injury. Dev Neurosci. 2006;28(4-5):364-379.
15.Dennis M. Language and the young damaged brain. In: Boll T, Bryant BK, eds. Clinical Neuropsychology and Brain Function: Research, Measurement and Practice. Washington, DC: American Psychological Association; 1989:85-124.

Working memory training has been shown to significantly benefit children and adults with ADHD (Attention Deficit Hyperactivity Disorder), Learning Disabilities, Traumatic Brain Injury (TBI), Stroke, Ageing and Epilepsy.

Working Memory has been called “the search engine of the mind”. An efficient working memory allows you to keep information online, manipulate it and use it in your thinking. It is responsible for delegating the things we encounter to the parts of the brain that can respond and take action. Working memory is therefore necessary for attention, staying focused on a task, blocking out distractions and keeping you updated and aware about what is going on around you in your environment.

It is working memory that helps us to perform efficiently and effectively in academic, professional and social settings. Working memory is required throughout our lives from our preschool days to our senior years. Without an adequate working memory preschoolers and infants school children would have difficulty learning the alphabet, remembering nursery rhymes, completing puzzles and following simple directions. Primary school children require an efficient working memory for reading comprehension, mental arithmetic and working independently in class and at home. High school and university students rely upon an adequate working memory to write notes in lectures, get a driver’s license, follow social conversations and academic discussions, writing reports and adhering to plans and timetables. For adults, working memory is essential for getting to work on time, meeting deadlines, prioritising multiple activities and handling conflicts within the family or social network. Without a functioning working memory to run things, seniors often find they become forgetful, get distracted easily, lose track of the topic of conversation and misplace important items such as glasses, keys, mobile phones.

In short, is it our working memory capacity that determines our cognitive performance and how quickly we learn new tasks.

The good news is that working memory can be trained! Learning Discoveries now offers the Cogmed Working Memory Training program

The Cogmed Working Memory Training Program is based on the work of Dr Torkel Klingberg and his colleagues at the Karolinksa Institute, Stockholm, Sweeden. The program is based on the neuroplasticity of the brain and several peer reviewed articles have been published in international journals over the past decade. Because Cogmed trains working memory, it changes the way the brain functions so that it can perform at its optimum capacity. This helps to create a platform for vital learning skills to develop.

Cogmed combines cognitive neuroscience with innovative computer games to improve attention problems caused by poor working memory. It consists of 25 training sessions, each 30-45 minutes long, over a five week period. Each session consists of a selection of various tasks that target the different aspects of working memory. The training is systematic and intensive. A qualified coach works with the trainee to provide structure, motivation and feedback on progress.

Research findings indicate that after Cogmed training children show improvements in the following areas: their assessment marks, remembering instructions, finishing assignments, working more independently, using appropriate social skills and the ability to take the initiative. For adults, results indicate improvements in focus, the ability to ignore distractions, remembering instructions, starting and finishing tasks, and improved planning.

Cogmed has been shown to significantly benefit children and adults with ADHD (Attention Deficit Hyperactivity Disorder), Learning Disabilities, Traumatic Brain Injury (TBI), Stroke, Ageing and Epilepsy.

To begin a Cogmed Working Memory Training Program, please contact us during business hours on (02) 9637 9998.

References
Klingberg et al (2002): “Training of Working Memory in Children with ADHD”. J of Clinical & Experimental Neuropsychology. Vol 24. No. 6, pp 781-791.
Klingberg et al (2005): “Computerised training of working memory in children with ADHD”. Journal of American Academy of Child and Adolescent Psychiatry. February, Vol 44, No.2 pp177-185.
Thorell et al (2008): “Training and transfer effects of executive functions in preschoolers. Developmental Science. Vol 12, No.1, pp. 1060-113.
Dahlin (2010): “Efects of working memory training on reading in children with special needs”. Reading and Writing. Vol24, No.4, pp.479-491.
Beck et al (2010): “A controlled trial of working memory training for children and adolescents with ADHD. Journal of Clinical Child and Adolescent Psychology. Vol 39, No 6, pp. 825-836.
Lundquist et al (2010): “Computerised training of working memory in a group of patients suffering from acquired brain injury”. Brain Injury. Vol 24, No. 10. pp. 117-183.
Johansson & Tornmalm (2011): “A controlled trial of working memory for patients with acquired brain injury: effects in daily life.” Scandinavian Journal of Occupational Therapy. August 15.
Diamond & Lee (2011): “Intervention shown to aid executive function development in children 4-12 years old.” Science. August 19. Vol 333, No.6045. pp.959-964.

In order for any drug to be approved by America’s Food and Drug Administration (FDA) only two randomly controlled trials showing drug superiority are required. Otto and Nierenberg (2002) found that despite the quantity of trials showing no significant improvements in symptoms, researchers can continue to alter treatment conditions and hypothesis and selectively choose the measurements that give the outcome their sponsors desire (Rising, Bachetti, Bero, 2008). Turner et al. (2008) reviewed 74 trials of 12 anti-depressant studies and in their meta-analysis found that anti-depressant studies with favorable outcomes were 16 times more likely to be published than those with unfavorable ones.

The study by Piggott, Leventhal, Alter and Boren (2009) conducted meta-analyses on efficacy trials that were submitted to the FDA including the STAR*D (Sequenced Treatment Alternatives to Relieve Depression) which is the largest and most expensive trial ever conducted. They found that the effectiveness of anti-depressants was even lower than the modest one reported by the study authors. The trial failed to report that the drop out rate was slightly higher than the group of participants, with drop rates increasing progressively across each study phase, due to negative side effects or suicidal ideation. It was also discovered that the measure of relapse required participants to be even more depressed than when they first commenced the trials, compromising the true rates of relapse.

Despite beliefs that anti-depressants are more enduring than placebo groups, Kirsch et al. (2002) found that while patients’ initial positive response to both decrease over time, the correlation was higher for anti-depressants (r=-0.84) than placebos (r=-0.62), indicating that the effects of anti-depressants diminish more rapidly than those of the placebo.

All of these studies aim to encourage the FDA to allow public access to all trials of a new drug, whether it has the sponsor’s desired outcome or not. They also specify that measures should not be changed in order to fit the hypothesis, and that a hypothesis is determined before the trials are carried out, to avoid publication bias (Piggott, Leventhal, Alter & Borren, 2010).

References
Kirsch, I., Moore, T., Scorbia, A., Nichols, S: The emperor’s new drugs: an analysis of antidepressant medication data submitted to the Food and Drug Administration. Prev Treat 2002; 5: article 23.

Otto, M., & Nierenberg, A: Assay sensitivity failed clinical trials for psychiatric disorders. Psychother Psychosom 2003:72: 115-127.

Piggott, E., Leventhal, A., Gregory, A., & Boren, J. (2010) Efficacy and Effectiveness of Antidepressants: Current status of Research. Journal of Psychotherapy and Psychosomatics, 79, 267-279.

Rising K., Bachetti, P., Bero, L: Reporting bias in drug trials submitted to the Food and Drug Administration: A review of publication and presentation. PLoS Med 2008: 358: 252-260.

Turner E, Matthews A, Linardatos E, Rosenthal R: Selective publication of anti-depressants trials and its influence on apparent efficacy. N Eng J Med 2008: 358:252-260.

Most assessment tools and research have focused on the diagnosis of Autism at the age of three, but what if we could diagnose autism before this age through the identification of subtle brain function signatures? Lead study author William Bosl, PhD, research scientist at Children’s Hospital Boston and instructor in pediatrics at Harvard Medical School, Boston, Massachusetts, told Medscape Medical News that they may have found a way to diagnose early developing characteristics of Autism Spectrum Disorder (ASD) in infants as young as 1 year, through the use of EEG (electroencephalogram) and basic algorithms.

It has been known for some time now that complex neurodevelopmental disorders are characterized by subtle brain function signatures early in life before behavioral symptoms are apparent. These EEG patterns or endophenotypes may prove to be measurable biomarkers for later cognitive impairments. EEG signals are thought to contain information about the architecture of neural networks in the brain on many scales. Therefore, detecting abnormalities in EEG signals as early as possible may turn out to be a useful biomarker for developmental cognitive disorders.

In this study, researchers set out to develop a biomarker for normal brain development.  Using resting EEG data and sophisticated algorithms (Multiscale Entropy or mMSE) to locate the density of neurons in particular areas of the brain and the connections between, they established a biomarker for normal brain function.. They then used this biomarker to distinguish typically developing children from a group of infants at high risk for autism spectrum disorder (ASD), defined on the basis of an older sibling with ASD.

The study collected data from 79 different infants, 46 of those were high risk for Autism (siblings diagnosed with autism) and 33 in the control group (no family history of neurodevelopmental disorders) and aimed to classify the children into high-risk or low-risk groups. Testing sessions included infants from ages 6 to 24 months. Resting EEG signals from the brain were recorded for all participants starting at 6 months and repeated when possible at the ages of 9,12,18 and/or 24 months.

Researchers were able to classify infants at the high-risk of Autism and in control group with 80% accuracy. Classification accuracy for boys rose to close to 100% at the age of 9 months and remained significantly high (70%-90%) at ages 12 and 18 months. For girls, the classification accuracy was highest at 80% at the age of 6 months, but declined thereafter to a non significant result at 12 months.

While EEG has predominantly been used with neurodevelopmental disorders such as epilepsy and seizures, the advances in technology has opened opportunities for EEG to be used to give more information about brain functioning. This study was the first demonstration of an information theoretic analysis of EEG data as a potential biomarker in infants at risk of a neurodevelopmental disorder.

The same researchers are currently testing 6-16 year-old children with autism and comparing their EEG patterns with the control. In future, they hope to follow up on the children who later develop autism and compare their EEG patterns. They encourage more studies to be conducted that will develop a greater understanding between neurological processes and cognitive function and hopefully develop a more clinically useful psychiatric biomarker for the identification of Autism and other neurodevelopmental disorders.

Reference

 William Bosl, Adrienne Tierney, Helen Tager-Flusberg and Charles Nelson  (2011). “EEG complexity as a biomarker for Autism Spectrum Disorder risk” BMC Med. Published online February 22, 2011.

The study was funded by grants from Autism Speaks, the National Institute on Deafness and Other Communication Disorders, and the Simons Foundation. Dr. Bosl reports being named on a provisional patent application that includes parts of the signal analysis methods used in the study. The other study authors have disclosed no relevant financial relationships.

L. S
Ashfield, December 2010

Dear Rosemary,

I am a mother of a 10 year old boy with Aspergers, ODD, ADHD, Anxiety and Learning Difficulties. My child was born in March 2000. The first 4 days of his life were bliss but after that it went pear shape. My son was very unsettled extremely difficult, hard to put to sleep, had bad reflux and so was difficult to feed to name a few things. And so began my road of searching for what was wrong. I tirelessly went to doctors, specialists and paediatricians who basically told me I was a neurotic first time mother. But I never gave up and continued to seek out anything and everything looking for help and answers.

The first year of schooling was a disaster as my child’s behaviour saw him on the naughty chair earning him the label of being the naughty child and I was the bad parent. This label did a lot of damage and took many years to undo. It was not until the end of 2006 at age six and a half did we finally get the diagnosis of an Autistic Spectrum Disorder which was later upgraded to all the above and suddenly it all made sense, but still no path I had crossed really helped my child.

Although we were extremely against medicating our child we relented nearly 12 months later towards the end of 2007 as I had seen first hand how difficult my child was at school. Initially the school reported what a difference the medication had made but as time went on I was not so sure and so began the experimental process with different dosages.

By 2010 we were now on our fourth school and had had several suspensions and I really knew this medication along with everything I was trying by way of intervention was not working and so began the experiment with different meds once again. We tried the “preferred” Ritalin but this only made things worse. This left me with the choice to either dope my child up or give him another medicine which is known to make children pile on weight.

As either option was not an option for us I decided to Google for an alternative DRUG FREE remedy. I came across Neurofeedback. I had two choices. A lovely man in Crows Nest, however, this is all he did or
Learning Discoveries in Harris Park run by Rosemary Boon who seemed to be a one stop shop as they offered a holistic approach. I went for the latter and on the 13th July 2010 (our first appointment),
Rosemary Boon became a big part of our lives and we have never looked back. In fact this is the only thing I have done for my child that actually worked.

It has now been only 5 short months but the change in my son is dramatic and seen across the home life but more importantly at school. He has better concentration and is able to apply himself and do his work and is overall more “normal” in his behaviour. As Rosemary put it herself my child was “Feral” when she first met him but she could see his softer side and she knew with a team approach we could help my little boy blossom – and he truly has.

I will not lie it was a huge commitment in both our time and financially but we feel it has been very worthwhile. Initially we did two appointments a day to really kick start his treatment and this meant time off school as well, but when he did return to school it was success all round. Of course we had our up and downs and I remember the school calling me up at lunch time to come and get him otherwise there may have been another suspension. I did this and rushed him out for an emergency appointment to Rosemary. The next day the school were in awe of Rosemary’s methods as it had made the most incredible difference in a positive way to my child’s behaviour.

I can not recommend Rosemary and her team enough. I guess if you are reading this then you need her help as well. My only advice would be to stop wasting any more time and start as soon as possible. Be open minded, be teachable to new ways and ideas especially to what you are eating and then sit back and enjoy the changes in your life as we have had.

GOOD LUCK!  You will be all the more better for finding Rosemary and her team.

Previous studies have focused on the physical effects of food, on conditions such as asthma, eczema and gastrointestinal problems. So where are the studies on the effects of food on the brain? The most recent study, published in The Lancet, February of this year by Pelsser, etc. (2011) investigated the effects of a restricted diet on behaviour of children with ADHD and differentiated between non-allergic and allergic mechanisms in food induced ADHD.

Children aged 4-8 years old who were diagnosed with ADHD, with no prior or current treatment, were separated into two groups. One group was given a restricted diet of foods limited to rice, meat, vegetables, pears and water with potatoes, wheat and fruits. The control group was maintained on a healthy diet.
Forty percent of children (40%) on the restricted diet showed significant improvement in their behaviour during the 5 week trial, in comparison to no improvements shown in children in the control group. The children who responded positively to the restricted diet were then re-introduced with either high or low IgG foods.

Sixty four percent (64%) of the children showed a significant behavioural relapse with the re-introduction of particular foods. The study found no direct relationship between the levels of IgG foods and the reduction of ADHD symptoms, however there was a positive relationship between a restricted diet and improvement in behaviour in children with ADHD and Oppositional Defiant Disorder. The study concluded that children who showed significant improvement in behaviour after a dietary intervention were most likely presenting with allergy-induced ADHD. The study recommended that all children with ADHD or ODD be placed on an elimination diet in order to define the foods that lead to allergy induced ADHD and other behavioural symptoms.

Reference:
Effects of a Restricted Elimination Diet on the Behaviour of Children with Attention-Deficit Hyperactivity Disorder (INCA Study): A Randomised Controlled Trial.
Lidy M Pelsser, Klaas Frankena, Jan Toorman, Huub F Savelkoul, Anthony E Dubois, Rob Rodrigues Pereira, Ton A Haagen, Nanda N Rommelse, Jan K Buitelaar. The Lancet February 5, 2011; Vol. 377: 494-502.

Two recent studies (2010) suggest that ADHD could be potentially misdiagnosed in nearly 1 million children in the USA simply because they are the youngest in their kindergarten class.

The first study by Dr Todd Elder, assistant professor of economics at Michigan State University, looked at a sample of nearly 12,000 children from the Early Childhood Longitudinal Study Kindergarten Cohort (June 2010). His results found that “the youngest children were significantly (60%) more likely to be diagnosed with ADHD and to be prescribed behavior-modifying stimulants such as Ritalin than their older classmates”.

According to Dr Elder, “the “smoking gun” was that the diagnoses depended on the children’s age relative to classmates and the teacher’s perceptions of whether they had symptoms”. He continued to say that there was “a big difference between a five-year-old and six- year old” and urged teachers and medical practitioners to take that into account when evaluating children for ADHD.

Furthermore Elder stated that, “medicating such children inappropriately was a cause for concern not just because of the effect of long term stimulant use on their health but also because it costs a lot of money and he estimated about 320 to 500 million US dollars is being wasted on unnecessary medication of young children for ADHD, of which 80 to 90 million is funded by Medicaid”. Finally, his study estimated that the overall misdiagnosis rate in the USA is approximately 1 in 5. This suggests that around 900,000 of the 4.5 million children currently diagnosed with ADHD have been misdiagnosed.

The second study (August 2010) which included researchers from North Carolina (NC) State University, Notre Dame and the University of Minnesota concurred with conclusions from the Elder study. Dr Melinda Morrill, co-author of the study and assistant professor of economics at NC State, found that children who were born after the cutoff date for kindergarten were 25% less likely to receive a diagnosis for ADHD when compared to their “relatively young-for-grade” peers” (i.e. those born just before the cutoff date). The study concluded that misdiagnosis in five year olds was due to lack of maturity and not because of “underlying biological or medical reasons,” (Morrill).

References
Elder, T.E (2010): “The importance of relative standards in ADHD diagnoses: Evidence based on exact birth dates.” Journal of Health Economics, In Press, Corrected Proof, Available online 17 June 2 010 DOI:10.1016/j.jhealeco.2010.06.003

Evans, W.N, Morrill. M.S., Parente, S.T. (2010): “Measuring Inappropriate Medical Diagnosis and Treatment in Survey Data: The Case of ADHD among School-Age Children.” Journal of Health Economics, In Press, Accepted Manuscript, Available online 4 August 2010.
DOI:10.1016/j.jhealeco.2010.07.005

Evidence is now mounting for the link between early exposure to pesticides and an increased risk of ADHD. A number of recent studies in the USA  indicate that early exposure to organophosphates or organochlorine compounds widely used as pesticides is associated with behavioural changes and attention problems at age five, and that the effects are stronger in boys.

A recent study published in the Journal of the American Medical Association (2010,  304: 27-28) looked at 1139 children and found that those with higher levels of exposure (measured by the concentration of chemical metabolites in urine) were twice as likely to have ADHD as those with the lowest exposure levels.

Researchers also found that those children with higher than medium exposures to pesticides had about a 20% risk of being diagnosed with ADHD. According to a recent US National Health and Nutrition Examination Survey, even children with relatively lower levels of pesticide exposure had a higher risk of ADHD.

Fruits and vegetables were the most common source of pesticide exposure in children according to Professor Maryse Bouchard of Sainte-Justine University Hospital Research Centre in Montreal, Canada. Her recommendation to parents was to buy organic or locally grown produce and to carefully wash fruits and vegetables to remove water-soluble chemicals.

In another longitudinal study, a team of  researchers at the University of California at Berkeley lead by Brenda Eskenazi, (professor of epidemiology and of maternal and child health)  followed more than 300 children to determine the effects of  prenatal pesticide exposure on a baby’s rapidly developing nervous system (Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS),.

The results suggest that “each tenfold increase in prenatal pesticide metabolites  was linked to having five times the odds of scoring high on the computerized tests of attention at age 5, suggesting a greater likelihood of a child having clinical ADHD. The effect appeared to be stronger for boys than for girls”.  This longitudinal study will continue to follow the children as they get older and the UC Berkeley researchers expect to present more results in the years to come.

Amy Marks, an analyst at UC Berkeley’s School of Public Health at the time of the study concluded that ” there is reason to be cautious, especially in situations where exposure may coincide with critical periods of fetal and child development.” (Aug 19, Environmental Health Perspectives-EHP ).

Genetics also increase the risk of developing ADHD  in vulnerable children. In a separate study published in the same journal (EHP) researchers found that 2-year-olds with lower levels of an enzyme (paraoxonase 1 (PON1) that breaks down the toxic metabolites of organophosphate pesticides, had more neurodevelopmental delays than those with higher levels of the enzyme.

Organophosphate pesticides are designed to attack the nervous system of organisms by disrupting neurotransmitters, particularly acetylcholine, which plays an important role in sustaining attention and short-term memory. Lead and phytates commonly used in toys and plastics have also been linked to ADHD. These studies add to the mounting evidence that chemical assaults on the most vulnerable in our society at critical periods of brain development can have disastrous effects on learning and behaviour.

“High levels of the symptoms of ADHD by age 5 are a major contributor to learning and achievement problems in school, accidental injuries at home and in the neighborhood, and a host of problems in peer relationships and other essential competencies,” says Stephen Hinshaw, professor of psychology and one of the country’s leading experts on ADHD, who was not part of this study. “Finding preventable risk factors is therefore a major public health concern.”

The Food Detective^TM Food Intolerance Test is designed for fast results, and looks at commonly eaten foods which may result in IgG antibody reactions. The symptoms of food intolerance can be delayed for many hours, even days and it can therefore be difficult to identify problem foods.

COMMON SYMPTOMS OF FOOD INTOLERANCE
Sufferers of food intolerances frequently complain of lethargy or “fogginess” and a general feeling of being unwell. A variety of the following symptoms may persist for years and many sufferers have has their symptoms dismissed by their doctor as being “all in the mind”.
These symptoms include:
-  Anxiety (acute & chronic)
-  Arthritis
-  Asthma
-  Bed wetting
-  Bloating
-  Coeliac Disease
-  Chronic fatigue Syndrome
-  Constipation
-  Cystic fibrosis
-  Diarrhoea
-  Fibromyalgia
-  Flatulence
-  Gastritis
-  Headaches
-  Inflammatory Bowel Disease
-  Insomnia
-  Irritable Bowel Syndrome
-  Itchy skin problems
-  Malabsorption
-  Migraine
-  Sleep disturbances
-  Water retention
-  Weight control problems

FOODS TESTED
If you test positive to any of the food groups listed below, the simple act of removing them from your diet can completely change your life!

Grains
-  Corn
-  Oats
-  Rice
-  Wheat
-  Durum Wheat
-  Rye
-  Gluten
-  Yeast

Beans & Legumes
- Cocoa Bean
- Soya Bean
- Legumes (Pea, Lentil & Haricot)

Meat & Poultry
-  Chicken
-  Lamb
-  Beef
-  Pork
-  Cow’s milk
-  Whole egg

Seafood
-  White Fish (Haddock, Cod, Plaice)
-  Freshwater fish (Salmon, Trout)
-  Shellfish (Prawn, Crab, Lobster, Mussel)
-  Tuna

Fruit & Vegetables
-  Apple
-  Blackcurrant
-  Broccoli
-  Cabbage
-  Carrot
-  Capsicum (Red, Green & Yellow)
-  Celery
-  Cucumber
-  Leek
-  Lemon
-  Grapefruit
-  Melon Mix (Cantaloupe & Watermelon)
-  Mushroom
-  Olive
-  Orange
-  Potato
-  Strawberry
-  Tomato

Nuts
-  Almond
-  Brazil Nut
-  Cashew Nut
-  Peanut
-  Walnut

Spices
- Garlic
- Ginger
- Tea

To make an appointment for the test or for advice on alternative foods please contact Rosemary Boon, Nutritionist via email or contact the office on (02) 9637 9998 during business hours.

Electro Magnetic Fields and Your Health