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Learning Discoveries Psychological Services
Rosemary Boon,
Registered Psychologist
M.A.(Psych), Grad. Dip. Ed. Studies (Sch.Counsel), Grad. Dip. Ed., B.Sc., MAPS

Telephone and Facsimile:
(02) 9727 5794

Email: rboon@iprimus.com.au


Postal Address:

P.O. Box 7120
Bass Hill NSW 2197


Submission to the Legislative Council of NSW

Standing Committee on Social Issues

Early Intervention (0-8 years) for Learning Disabilities including ADHD/ADD

Multi-modal intervention strategies

*This submission was made to the Standing Committee on the 22nd of January 2001*

ABSTRACT

Specific Learning Difficulties/Disabilities (SLD) and attentional and behavioural problems (Attention Deficit Disorder with and without hyperactivity (ADD/ADHD) are neurological disorders which if left undiagnosed and untreated have enormous social implications. It is the aim of this paper to inform the committee of the recent scientific findings and to propose a model which assesses the multifaceted nature of these disorders including metabolic, neurological and physiological factors so that the underlying biological conditions are treated rather than continuing with the pharmacological paradigm which merely masks the symptoms with a variety of neurotoxic medications. While the effect of these disorders are far reaching for the individual and their quality of life, they have major impacts on society as a whole. They have a stratifying socio-economic impact with associated losses in productivity, increased costs of medical care and education, escalating substance abuse, criminality and the social costs of treating all these ailments.

This group who suffers from learning difficulties and ADHD may, through the search for answers to their disorders, light the path to improved mental and physical health for every industrialised nation in the world, through identification with antibody testing, dietary and neuro-physiological intervention. It is an issue with huge social implications, and for that reason alone, warrants thorough investigation. Such investigation would necessitate an interdisciplinary panel consisting of experienced and qualified professionals in the fields of psychology, psychiatry, neurology, general medical practice, education and nutrition who are already using this model, as well as parents and members of the wider community including business leaders. Once the underlying causes of these disorders are addressed, the prognosis for children with SLD and ADD/ADHD improves remarkably.

Table of Contents

 Introduction

  Definition of Specific Learning Disability

  DSM IV* Criteria for ADHD

  Incidence & Common features of Dyslexia, ADHD & Dyspraxia

  Comorbidities with ADHD and Learning Difficulties

  Adolescent and Youth Outcome

  ABS** Statistics on Mental Disorders including Depression

  Mental Disorders and Suicide

  ABS** Statistics on Literacy and Unemployment

  The Medical Model

  Learning Pyramid Model

  The Functional Medicine Model

  Assessments and Interventions

  Quantitative Electroencephalography (QEEG)

  Neurofeedback (EEG biofeedback)

  Diet and Nutrition

  Gluten-Dairy Connection with Learning Difficulties, ADHD & other disorders

  Food Additives/Chemicals

  Nutritional Supplements

  Genetically Modified Foods

  The Role of Essential Fatty Acids Supplementation

  The Role of Neutraceuticals

  The Role of Vitamins

  The Role of Adequate Water

  Central Auditory Processing Disorder (CAPD)

  SAMONAS Sound Therapy

  Lindamood-Bell for the remediation of reading, spelling , comprehension

  Primitive Reflexes

  Discussion on the impact of LD and ADHD

  Recommendations

  Interviews and Assessments

  Educational Interventions

  Health Interventions

  Interventions for Parents

  Interventions for the Food Industry

  Summary

  Conclusion

  References

  Appendix A- DSM-IV Criteria for ADHD

  Appendix B- Adverse effects of Stimulant Medication

  Appendix C- Journal References for EEG biofeedback in the treatment of Learning Disorders, ADHD and Epilepsy

  Appendix D- Food additives known to cause side effects

  Appendix E – The relationship between marijuana and ADHD

 

* DSM-IV Diagnostic and Statistical Manual published by the American Psychiatric Association

**ABS Australian Bureau of Statistics

Introduction

Rosemary Boon Reg. Psychologist
M.A.(Psych), Grad. Dip. Ed. Studies (Sch.Counsel), Grad. Dip. Ed., B.Sc., MAPS

Member of The Australian Psychological Society, Australian Guidance and Counselling Association,
Counsellors and Psychotherapists Association of NSW, SPELD, SSLDSG,
Society for Neuronal Regulation, Affilliate of EEG Spectrum USA.

Rosemary Boon is a registered psychologist, teacher and trainer. She has worked in the fields of special education and school psychology for over 20 years in both government and private schools in the Metropolitan South West Region of Sydney. Her work as a school counsellor focused on children with learning and language disabilities, attentional deficits, and behavioural and emotional problems. This led her to look for better ways to help them. To this end she has travelled extensively to gather knowledge and skills learning from world pioneers in their field, and continues to do so. Further training has included the Lindamood- Bell Method (Sans Luis Obispo, California), Accelerated Learning Techniques, The Spalding Method, Neurofeedback (EEG Spectrum USA), SKIL QEEG Topometric Analysis (USA), SAMONAS Sound Therapy (UK, Germany), The Listening Program (UK), Hypnosis, NeuroDevelopmental Therapy and Flexyx Neurotherapy (USA). She is currently undertaking further studies in clinical nutrition.

Over the past ten years, Rosemary has developed her private practice to cater for the needs of children and adults with Learning Disabilities and ADD/ADHD. Her unique blend of psychology, effective researched based teaching methods and state-of-the-art multimodal therapies have proven to be powerful remediation tools for those who have failed to improve with other methods and therapies. Inter-therapist referral is undertaken when appropriate.

Rosemary is a strong advocate for the rights of individuals with disabilities and in her practice she endeavours to encourage and empower her clients by remediating their difficulties and nurturing their talents so that they fulfil their potential and therefore become their own best advocates. She is a member of several professional organisations and is currently President-elect for the Ausrtalian Chapter of the Society for Neuronal Regulation (SNR), a society devoted to the study and practise of neurofeedback.

Her comprehensive range of services include:

 

Early Intervention (0-8 years) for Learnisng Disabilities and ADHD/ADD – Multi-modal intervention strategies- Rosemary Boon, Psychologist (02) 9727 5794

In reference to the Legislative Council of New South Wales’ Standing Committee on Social Issues, in their current inquiry into Early Intervention into Learning Difficulties during the early childhood years (ages 0-8), it must be understood that the term learning difficulties covers a broad spectrum of disorders. For the purpose of this paper only three of the more prevalent disorders will be considered viz. Attention Deficit Hyperactivity Disorder (ADHD), dyslexia and dyspraxia. Since there is a considerable overlap of these conditions a range of outcome-based multi-modal interventions is necessary.

Therefore, the current diagnostic procedures for learning disabilities and ADHD, and the therapeutic interventions currently used to manage these conditions will require a significant paradigm shift by the medical profession in particular, by special learning disabilities teachers, classroom teachers, some educational psychologists including school counsellors, parents and the community in order for society to give these children a fighting to achieve their potential without the need for stimulant medication.

This submission offers an alternative perspective and safe and effective non-pharmacological treatments and strategies for teachers and parents who must work and live with the children in their charge, but who recognise the fallacy underlying the current practice of administering powerful medications to children, in the absence of a clear and full investigation and understanding of the condition being treated, or the therapeutic action of the drugs administered.

Definition of Specific Learning Disability

A Specific Learning Disability (usually abbreviated to LD) means a disorder in one of more of the basic psychological processes involved in understanding or in using language (spoken or written), which may manifest itself in an imperfect ability to listen, think, speak, read, write, spell or to do mathematical calculations. It also includes directional confusion, sequencing difficulties, and short-term memory retention problems and inefficient working memory. These problems are NOT primarily due to visual, hearing or motor handicaps, NOR due to mental retardation, emotional disturbance, or because of environmental, cultural, or economic disadvantage. The individual is considered to have a LD if achievement is not commensurate with age and ability levels in one or more of the above specific areas when provided with learning experiences appropriate for age and ability levels [1].

DSM IV Criteria for ADHD

The Diagnostic and Statistical Manual of Mental Disorders (DSM IV) published by the American Psychiatric Association (1994), characterises ADHD by four sets of features and one broad form of differentiation including hyperactivity and impulsivity, or inattention, which interfere with social, academic or occupational function; and which appear in two or more settings. Some of this impairment is required to have been present prior to seven years of age [1]. Appendix A (page 47) contains the fully DSM-IV Criteria for this disorder. Despite some semantic difficulties, this delineation of features identifies a very real and debilitating problem that most classroom teachers see daily and parents and families have to live with. It is hoped that when the committee finishes reading this paper it will truly understand and appreciate the depth and magnitude of this disorder.

Learning difficulties which arise from the above definitions therefore include dyslexia, dyspraxia, Attention Deficit Disorder (ADHD), central auditory processing disorders, visual processing disorders, receptive, expressive and pragmatic language disabilities, speech and articulation disorders, and working/short-term memory deficits.

Incidence & Common Features of Dyslexia, ADHD & Dyspraxia

Current research suggests that up to 20% of children experience problems with their schooling at some stage and that approximately 5% suffer from disabilities severe enough to interfere with normal progress. The incidence of ADHD is reported to be between 2% to 10%. Furthermore, most studies suggest that between 25 and 40 percent of individuals with learning disabilities have inherited this from their families. However, while the familial pattern appears to be clear, the genetic process is not yet clear [2-3]. It is not uncommon to find a family where one child has ADHD (difficulties with sustained attention, impulse control, hyperactivity and reward deficiency which leads to addictions), another dyslexia (difficulty with reading, spelling and writing) and a third dyspraxia (impairment or immaturity of the organisation of movement and often associated with problems of speech and language, perception and thought). It is also quite common for an individual to suffer from more than one of these conditions [4].

In fact:

Table 1.

ADHD, DYSLEXIA AND DYSPRAXIA – COMMON FEATURES

  • Neurodevelopmental anomalies

Pregnancy and birth complications

Low birth weight, reduced head circumference

Minor physical anomalies

  • Excess of males affected
  • Allergies/autoimmune problems
  • Other physical complaints, such as stomach ache and migraine
  • Motor coordination problems
  • Sleep problems
  • Mood disorders – depression, mood swings
  • Behavioural problems- hostility, stress-aggression, impulsivity, hyperactivity
  • Perceptual and cognitive abnormalities- visual and auditory processing problems, attention/working memory deficits

Source: Stordy and Nicholl "The LCP Solution" Pg7 [4]

Given that most cases of ADHD are misdiagnosed, it is important to differentiate ADHD from other potentially applicable disorders. It is now accepted in research and clinical practice that children may and often do have multiple disorders coexisting with their ADHD at the time of initial clinical presentation. Such comorbid disorders may interact with and exacerbate each other, resulting in different developmental courses and adolescent and adult outcome, have somewhat different pattern of causes, and even a different response to treatment, than just ADD alone. [2, 5-9, 155-158]. See Table 2. for further figures relating to comorbid (co-occurring) disorders.

Table 2.

COMORBIDITIES WITH ADHD/ADD AND LEARNING DIFFICULTIES

Psychiatric Disorders:

Oppositional Defiant Disorder (ODD) more than 60%

Conduct Disorder (CD) more than 45%

Antisocial - Delinquent Tendencies more than 25%

Anxiety Disorders 30%

Major Depression 30%

Somatisation (thought) Disorder is present in 24-35% of 12-16 year olds who have difficulties with cause-effect perception, lack empathy, are emotionally labile, capricious and display unpredictable mood swings and atypical motor mannerisms

School/cognitive Problems:

Under-Productivity or achievement in schoolwork 90%

Excessive Variability of school work and Learning Disabilities (25-35%) which lead to lower IQ over time

Emotional Problems:

Immaturity 50% which includes over-reaction to stimuli, low frustration tolerance

Poor self esteem 65%

Social Skills Problems:

Immature play/social interests 50% with little regard for social consequences, rejection from peers due to intrusive behaviour, selfishness and misperception of intent of others

Developmental/Medical Findings:

Immature motor coordination 30-60%

Greater enuresis/encopresis (bedwetting and soiling)10-20%

Increased sleep disturbances 30%

Source: Russsell Barkley, 1995 Sydney Conference on Attention Deficit Disorder [158]

Implications of Unresolved Learning Disabilities and ADHD

Research studies [11b, 12-13, 69, 158-168] indicate that for teenagers with ADHD, the absolute level of symptoms declines, although 70-80% continue into adolescence with the full range of ADHD symptoms. 50-60% of these adolescents will continue to display ADHD characteristics in adulthood. Table 3. summarises the adolescent and young adult outcome. Predictors of adult outcome include:

  1. Family socio-economic status (predicts work success and academic outcome)
  2. Child's intelligence (predicts educational achievement)
  3. Degree of childhood conduct problems (especially early lying, stealing and also predicts social, legal and academic outcomes)
  4. Degree of peer relationship problems (predicts ongoing social problems)
  5. Extent of parental psychopathology (predicts extent of child psychopathology).

Only 11% of ADHD children are free as adults of any psychiatric diagnosis, function well and have no significant symptoms of their disorder [12,167,168].

Table 3.

ADOLESCENT AND YOUNG ADULT OUTCOME OF ADHD

Many teenagers will go on to develop:

Conduct Problems:

25% will develop anti-social personality disorder

25-35% will abuse alcohol/marijuana/cocaine or some other drug and

10-15% of these teenagers will continue with substance abuse into adulthood

20% will exhibit physical aggression

3 times as many changes of residence as normals

3 times as many car accidents as normals

4 times as many traffic citations

50% will be involved with the police

20% will appear in court as a result of police involvement

Emotional problems:

10% will have attempted suicide in the past 3 years

20% will experience sexual dysfunction

65% will experience a low self-esteem

Most of them are often demoralised

Social problems:

75% who report more interpersonal problems than normals

Appearing less assertive

Being less skilled in heterosexual relationships

Having fewer close friends than normals

Educational attainment as a result of ADHD:

35% fail to finish high school

20% fail to persist past high school

5% will graduate from university compared to 41% of normals

25-35% will have repeated a grade in school

More school expulsions especially if ODD or CD

Learning problems persist

Employment functioning as a result of ADHD:

As teenagers they function as well as others on the job, if it is unskilled

As adults, they are rated as significantly worse in job functioning

Work less well independently

More likely to be "laid off "or quit

Changes of jobs more frequent

Many are independent and self-supporting.

As a group, they are likely to be less educated and under-employed ADHD continues to affect the fabric of daily living in most cases.

(Source: Barkley, Sydney 1995 [158] and others[2, 5-9, 12, 159-168, 182-183])

From these facts and figures one can see that the prognosis (outcome) for children with SLDs and ADD/ADHD is not good. They are at greater risk of illiteracy, unemployment, social maladjustment, depression, anxiety, obsessive-compulsive disorder and other mental and physical disorders (asthma, cancer, diabetes, and food allergies). It is therefore necessary to stress the seriousness of these conditions and the cost to the community if the essential and effective interventions outlined in this document are ignored.

In an effort to highlight the issues of quality of life and the rights of people with mental disorders, one needs to look at figures published by the Australian Bureau of Statistics (ABS) [145] and in particular a statement from an article entitled "Australian Social Trends 1999" [146]

"For society, mental disorders represent a major expense through loss of productivity and the costs of treatment. For the individual, it can affect the ability to work and participate fully in society. In addition, individuals may feel isolated and discriminated against due to the attitudes of many people who are uninformed about the nature of mental disorders. In a severe form, this may lead to suicide"[146].

ABS ** Statistics on Mental Disorders including Depression

The 1997 ABS mental health survey reported that 2.4 million people over the age of 18 years (18% of all adults) had experienced a mental disorder during the past 12 months before the survey was conducted. The three categories of mental disorders that were most prevalent were:

  1. affective disorders (depression, dysthymia, mania, hypo mania and bipolar or manic depressive illness)
  2. anxiety disorders (panic disorders, agoraphobia, social phobia, obsessive-compulsive disorder, generalised anxiety disorder and post traumatic stress disorder)

(3) Substance-use disorders (alcohol, illegal and prescription drugs, cigarettes, marijuana) [145].

Young adults (18-24 years) had the highest prevalence of mental disorder (27%) according to the 1997 ABS report handed to the Federal Minister for Health and Family Services, Dr Michael Wooldridge [150]. Highlights from this report include:

The ABS continues to state that the presence of a mental disorder may predispose individuals to other disorders. Depression is recognised by the World Health Organisation as a disease of "major and growing proportions which will be the second largest cause of years of life lost due to disability and mortality in the year 2020" [146]. It is an acknowledged fact that combinations of disorders have a cumulative effect on the level of mental dysfunction. One can only speculate as to whether the planners of the Depression Action Plan formulated in 1999 were even aware of the existence of the scientific data supporting neurofeedback and dietary interventions as outlined in this submission.

Table 4 highlights the suicide trends for those with mental disorders.

Table 4.

MENTAL DISORDERS & SUICIDE

ABS figures [145] indicate that people with mental disorders were:

  • 4 times as likely to have thought about suicide since the age of 18 as people without a mental disorder (37% compared to 9%).
  • 7 times more likely to have attempted suicide (10% compared to 1.5%).
  • In 1997, suicide ranked fourth in terms of the years of potential life lost before the age of 76.
  • In 1997, the rate for suicide jumped 12% from the previous ten-year period to reach 14.7%.
  • 50% of all suicides occur in people under 35 years of age. These statistics include suicide rates for children 10-14 years.
  • The suicide rate for men is 4-5 times higher than that for women. Firearms, death by hanging and strangulation are common methods used by men.
  • Canadian statistics during the period 1993-1997 indicated that 229 children aged 5-14 years completed suicide and that 2 of these children were boys under 10 years. Of the remaining 227 children, 155 were male and 72 were female. Highly lethal methods such as guns and hanging accounted for over 90% of suicides [148].
  • 46% women used health services (most commonly a general practitioner) compared to 27% men.

 

Table 5.

POTENTIAL RISK FACTORS FOR SUICIDE

Mental disorders- particularly affective (mood) disorders such as depression and bipolar disorder.

Comorbidity (co-occurrence) of mental and alcohol and substance abuse disorders

Other psychiatric disorders

Hopelessness

Impulsive or aggressive tendencies

Barriers to accessing mental health services

Isolation, a feeling of being cut off from other people

Poor coping strategies

Poor social adjustment

Family problems or familial suicide

History of suicidal behaviour

Chronic health problems

Relational, social, work, or financial loss

Easy access to lethal methods, especially guns [148-149]

 

Readers will easily identify these factors are most prevalent in the learning disabled/ADHD population.

Furthermore, "it is widely accepted that socio-economic status affects health" states the Australian Social Trends 1999 paper on "Health and socio-economic disadvantage of areas[147]. It continues to say that ‘there is a substantial body of evidence that people of lower socio-economic status have worse health than others". The five most common ailments in this group are arthritis, asthma, bronchitis/emphysema, ulcer and diabetes. Deaths from bronchitis/emphysema, pneumonia/influenza, lung cancer, diabetes, cerebrovascular disease (strokes), suicide and traffic accidents are higher in more disadvantaged areas. The report concludes that "people from more disadvantaged areas were less likely to have taken less preventative health actions", "were least likely to have private health insurance (24% compared to 61% in more affluent areas)" and the pattern of greater use of certain medical services confirms that of other studies and is consistent with people from disadvantaged areas having poorer health"[147]. Thus with the introduction of the GST on food items, particularly health foods and nutritional supplements, the problem can only worsen.

The majority of drug offences [152] involved cannabis (76.9%) and an increase of 22% was noticed for heroin with 12.3% of offenders being prosecuted for this offence. It will be shown in this paper that the ADHD brain is a "craving brain" and addictions are an attempt at self-medication.

ABS Statistics on Literacy & Unemployment

The rate of participation in the labour force (ie. being either employed or unemployed, rather than not participating at all) by persons aged 25-65 is clearly related to literacy levels. The 1997 ABS [151] survey objectively assessed three types of literacy:

Table 6. highlights the relationship between literacy and unemployment.

LITERACY AND UNEMPLOYMENT

44% of Australians had literacy skills in the very poor (Level 1) and poor (Level 2) bands for prose;

44.8% of Australians had literacy skills in the very poor (Level 1) and poor (Level 2) bands for document literacy

43.3% of Australians had literacy skills in the very poor (Level 1) and poor (Level 2) bands for quantitative literacy

Of those aged 16-65 who are in the labour force, those with low literacy skills have a greater chance of being unemployed than do those who are highly skilled.

The unemployment rate for the former group (low skills) was 11.3%, more than double that of the latter - 4.6%.

Among people aged 25-65 who are employed, those with higher literacy skills generally earn more than those with lower skills. In Australia, 58% of employed persons with good/very good prose skills are in the top 60% of earners [151].

Given the fact that many children with learning difficulties and ADHD slip through the education system and leave school undiagnosed, accurate assessment is vital and the current model used for diagnosis is insufficient because it ignores the underlying conditions. A shift away from the pharmacological paradigm, in recognition of the multifaceted nature of these disorders is therefore prudent. In contrast to the medical model which is outlined below, the multi-model approach described herein does not rely on symptom-suppressing drugs, but rather on more safe, natural therapies to address the critical underlying causes of the disorders, which when addressed, greatly improves the long-term prognosis for children with learning disorders and ADHD.

The Medical Model

Paediatricians and psychiatrists make a diagnosis of ADHD based on teacher and parent questionnaires (The Child Behavior Checklist; The Child Attention Problems Scale; The ADHD Rating Scale; The School Situations Questionnaire, and The Connors Teacher Rating Scale-Revised).

It must be noted that the aim of stimulant medication prescribed for ADHD children is to relieve or suppress the unwanted symptoms of the disorder (hyperactivity, impulsivity, distractibility, forgetfulness, oppositional behaviour) and is NOT a cure. This is similar to taking Aspirin for pain relief.

Furthermore, since the medication is short lived in the body (approximately 4 hours) repeated doses throughout the day are necessary as symptoms return once medication is reduced. Additionally, the body builds up a tolerance level to the medication and thus progressively higher doses are needed to achieve the same results. More importantly, these drugs were approved decades ago before their long-term effects on young children whose brains are still developing could be studied and have yet to be fully established.

The most popular stimulant medications prescribed for learning difficulties and ADHD are methylphenidate (Ritalin), and Dexamphetamine, members of the amphetamine family and closely related to cocaine. The widespread popularity of stimulant drug abuse has provided a sad opportunity to study the effects on the brains and cardiovascular systems of young people [10, 16, 27-32]. Single photon emission computed tomography (SPECT) studies by neurologist Daniel Amen and his colleagues in the USA have shown significant deterioration in brain anatomy following long term use of stimulants [16]. Cylert, the non-amphetamine stimulant has resulted in severe liver failure in several children [10, 33, 34] whilst Norpramin (desipramine) and imipramine, the antidepressants often used as an alternative to stimulants, have caused sudden death in many children [35]. Prozac and its close relatives are also being prescribed to children, despite the fact that they have not been approved for use with this age group [10] and isolated reports of very serious harm have begun to emerge [36].

While evidence supports the short-term efficacy of stimulant medications in ADHD, such therapies are inadequate, shortsighted responses to this pervasive problem that afflicts from 2% to 10% of school children. Several follow-up studies of subjects who underwent lengthy courses of stimulant therapy, have failed to show significant long-term benefit from such therapies [11a & b]. This absence of long-term benefit may also be seen through comparing a 15 year follow-up of 63 hyperactive children who were not treated with stimulant therapy [12] and a 12 year follow-up of 60 children, most of whom had undergone stimulant therapy [13]. Both groups had fared equally poorly when contacted at follow-up. Evidence of an associated delayed maturation of parts of the brain involved in executive function until the third decade of life, has also been reported [14-15].

If one reads the relevant literature, it is hard to deny that stimulant therapy offers a very effective focussing and settling agent to aid in classroom management, and that this furthers the interests of the afflicted child’s classmates, their teachers and parents searching for an effective means to manage a difficult child, and the shareholders of multinational pharmaceutical manufacturers, while offering little benefit to the learning disabled/ADHD child.

Subjecting children to toxic pharmacological interventions (some of which have never been approved for use with children) is the path of least resistance for those involved and has life-long implications and consequences. It should therefore be based upon a much more solid foundation than a parent or teacher’s observation rendered in ignorance of the critical and differentiating features of ADHD.

Much of current medical practice involves simply prescribing the "right drugs" without carefully evaluating the outcome of that treatment (including change in symptoms, side effects and quality of life) [10]. Little if any attention is paid to developmental and family histories or other relevant presenting conditions. This very dangerous practice of placing very powerful neurotoxic and cardiotoxic drugs as "band- aids" on symptoms without an understanding of the underlying cause of those symptoms carries the potential for serious side effects. Some of the known side effects of stimulant medication have already been discussed and are summarised in Appendix B (Page 48). Concern over this practice is growing in the USA as well as here in Australia. Steven Hyman, director of the National Institute of Mental Health (NIMH) Rockville, USA asks, "How can we tolerate a situation in which drugs are prescribed to an increasing number of preschoolers without safety and efficacy data? [46]. This concern is echoed by Michael Lyon, MD and author of "Healing the Hyperactive Brain through the New Science of Functional Medicine" when he states:

"If we should learn one thing from the history of toxicology it should be this: any substance known to kill brain cells or damage the heart over the short term, must be highly suspect for long term toxicity with regular exposures that are even a small fraction of the amount which causes short term harm"[10].

It was concerns such as these that had led to the Class Action Law Suit against Ciba-Geigy/Novartis (manufacturers of Ritalin) and against the support group Children and Adults with Attention Deficit Disorder (CHADD) in the United States. The suit alleges fraud and conspiracy. It states that from approximately 1955 to 1995 the manufacturer planned, conspired, and colluded to create, develop and promote the diagnosis of ADHD in a highly successful effort to increase the market for Ritalin " [http://www.ritalinfraud.com/]. It achieved this through (1) actively promoting Ritalin as the "drug of choice" to treat children with ADHD, (2) actively supporting co-defendant groups such as CHADD, both financially and with other means so that such organisations would promote and support the ever increasing implementation of ADD/ADHD diagnoses as well as directly increasing Ritalin sales, (3) distributing misleading sales and promotional literature to parents, schools and other interested persons in an effort to increase the diagnosis of ADHD and sales of Ritalin.

From 1991 to 1994 CHADD received $748,000 from Ciba/Novartis in a "deliberate effort to increase the sales of Ritalin, and to increase the supply of methylphenidate (the generic name for Ritalin) available in the United States, and to reduce or eliminate laws and restrictions concerning the use of Ritalin and methylphenidate in the United States, all to the financial benefit of Ciba/Novartis. Ciba/Novartis made such financial contributions with the purpose of advertising and promoting sales of Ritalin – an internationally controlled substance. Ciba/Novartis has thus repeatedly violated Article 10 of the of the United Nations Convention on Psychotropic Substances, 1019 U.N.T.S. 175 (1971)" The full article can be found at the Ritalin Fraud website: http://www.ritalinfraud.com.

Despite these concerns, a recent article in the Washington Post (January 2, 2001) states that a clinical study to determine the effect of Ritalin on 312 severely afflicted ADHD children under the age of six will commence this month. The Preschool ADHD Treatment Study (PATS) organised by Laurence Greenhill of the New York State Psychiatric Institute at Colombia Presbyterian Medical Centre says the study will last 40 weeks and is necessary "because it’s been shown that more and more children in this age group are receiving this medication and we don’t have any idea about safe dose range or how it works over time" [46]. Hyman says that without a controlled trail "in essence every kid is an uncontrolled experiment---but we never learn anything". This trial raises ethical questions including "whether children this young should be subjected to clinical trials of any drug, much less one with Ritalin’s ability to alter the way the brain works, possible effects on a young child’s developing brain and whether little children can adequately understand their participation and articulate their willingness to take part in any clinical trial" [46].

The Learning Pyramid Model


Figure 1.

Learning disabilities and ADHD are multifaceted, life-long difficulties and they will require multi-modal interventions and on-going management and support. The model above (Figure 1) is based on the latest research from cognitive psychology and brain studies, blended in a unique way to accommodate diverse learning styles and individual needs. Experience has shown that much effort, time and money is wasted when the order of the model is not followed or when certain steps are missed. This model which has been used in this clinic since 1996 is closely aligned to the Functional Medicine Model (Figure 2) being adopted by growing numbers of medical practitioners in the United States [10].

Figure 2. Source: Michael Lyon, MD "Healing the Hyperactive Brain" Page 2, 2000 [10].

Using these models learning disabilities and ADHD are conceptualised as complex, multifactorial, neurological disorders, which are often the result of a collection of underlying physiological conditions and which can be modulated by environmental factors. There is a series of antecedent events, triggers and mediators that are common to both.

Antecedent events or risk factors which predispose an individual to the development of symptoms of learning disabilities and ADHD include: genetic factors, factors which begin at conception, during pregnancy or during infancy and early childhood; environmental and dietary toxins; head injury or stresses within the family. These factors set the stage for physical imbalances and internal disorders by weakening a person’s basic physiological and neurological foundation.

Triggers are physical or biochemical problems arising out of the weakened or susceptible physiology in a person with various antecedents that have been exerting stressful influences upon organ systems, cells or molecules. Common triggers are food allergies (wheat, rye, barley, oats, cow’s milk, yeast, eggs, corn, soy, chocolate, peanuts, oranges, artificial colours and preservatives), intestinal parasites (Candida Albicans, Giardia, Cryptosporidium, Helicobacter pylori, Entamoeba hystolytica) or chronic infections (ear infections, otitis media, upper tract respiratory infections, etc), and inadequate diet, poor sleeping patterns and lack of exercise. In other words the "whole child" needs to be the focus of intervention rather than just their presenting symptoms.

The triggers in turn lead to imbalances of other critical substances known as mediators. The disturbed mediators in ADHD are primarily the brain neurotransmitters dopamine, serotonin and norepinephrine. Imbalance in these biochemical mediators then leads to the signs and symptoms of ADHD and learning difficulties [10].

The search for these antecedents, triggers and mediators needs appropriate investigation when a client/patient is referred. It usually involves several visits to specialists, sophisticated laboratory testing (some of which is not currently available in Australia and hence the cost factor prohibits low-income earners from access) and extensive parent, teacher and community education.

However, there are several barriers in our society, that currently prevent the adoption of such a model. Our culture relies upon paediatricians and teachers to render accurate diagnoses, effective treatment and appropriate instruction. Given the models outlined, this expectation may exceed reality. The risk of misdiagnosis, along with a singular reliance upon stimulant therapy, simply constitutes a short-term masking of the symptoms of physical ailments, and of the underlying causes of what may constitute most cases of learning difficulties and ADHD.

The medical community is steeped in convention and tradition and has yet to acknowledge these possibilities and embrace the shift in paradigm that is required to adopt these models. "The majority of those in mainstream medicine are quick to show their bitter opposition to any form of "alternative" or "complementary" medicine dismissing or refusing to read the published literature in peer reviewed journals and research studies on natural therapies whilst failing to recognise that most of what they practice is not based on solid scientific evidence" says Michael Lyon, MD"[10].

Lyon continues to say that studies have shown that the majority of physicians are greatly influenced by the marketing efforts of drug companies and may obtain as much as 90% of their continuing education through pharmaceutical representatives and drug company sponsored educational programs. It is also a well-known fact that the present drug approval system is greatly influenced by the profits that can be gained by obtaining drug approval[10].

Furthermore, nutrition is not taught at medical school and therefore many practitioners are ignorant of effective strategies in this area and dismiss the importance of nutrition in the care of their patients. Additionally, once a particular treatment has become widely accepted, it can become heresy to question the correctness of this therapy. This active opposition by the medical establishment has resulted in a scarcity of research dollars to support the study of treatments which cannot be patented, making the personal price too high for most researchers wishing to conduct research into non-conventional treatments.

Some teachers in Australia are fast emulating their American counterparts who support the process that leads to stimulant therapy. Stimulant drugs offer to aid the teacher in controlling classes through improving the behaviour and performance of most children, not just those who suffer from learning difficulties or ADHD. Some learning difficulties support groups are also strong advocates in promoting the medical model. It is currently estimated that about 50,000 Australian children including preschoolers are prescribed stimulant medication.

Given the current political context where class sizes continue to grow, and teacher performance is measured by student performance on standardised testing and completing an academic curriculum and where student manageability is likely to be aided by stimulant therapy, it is very tempting for the teachers and parents to simply nod assent in a complex diagnostic process, rather than oppose the powerful, popular following that supports such diagnostic and therapeutic practices. The magnitude of learning and behavioural problems which are often associated with learning disabilities and ADHD can serve as a powerful inducement to teachers and parents looking for a "quick and easy fix" to accept any answer, whether temporary or not. This is understandable since many parents who have tried traditional behavioural management techniques and conventional tutoring methods find themselves in desperate need of respite. Since there is currently no "gold standard" for diagnosing ADHD, diagnosis is usually based on teacher and parent evaluations, which often leads to stimulant medication being prescribed.

This blind partnership with medical clinicians obscures issues of accountability. Each participant, whether parent, teacher or physician, is placed beyond reproach in the current situation. It also provides an easy escape from responsibility to medical and teaching professionals involved in the diagnostic process. The current status quo is that teachers and parents are pressured into participating in a diagnostic process about which they usually know very little. However, when these critical underlying factors are identified and dealt with effectively, the results are often extraordinary and the long-term prognosis for the learning disabled/ADHD child may be greatly improved.

Proponents of natural medicine in Australia, like their American counterparts have long struggled for recognition. The Australian natural medicine summit of 1996 resulted in the creation of a special division within the Therapeutic Goods Administration that eventually became a statutory body in its own right. This was a major step forward in the recognition of natural medicine by government and of its acceptance in the general community.

On 5th October 2000, the White House Commission on Complementary and Alternative Medicine under the chairmanship of Dr James S. Gordon, Professor of Georgetown Medical School advised the President that

"a huge percentage of people in this country (America) are using complementary and alternative therapies as a significant part of their health care" and that "when it comes to people facing life-threatening illness, the number goes up"[45].

This commission is not only concerned with the perceived benefits but is also charged with suggesting specific policies for natural medicine integration within the overall health care system. It will also look at ways of providing consumers the kind of information they need in order for them to discriminate between approaches that may be effective and those that may be harmful. The commission will also look at the kind of education to be provided to medical students, psychology students and students of naturopathic medicine. It will be most interesting to learn of their recommendations to President Bush.

In Australia, psychometric assessments for central auditory processing disorders, neuropsychophysiological assessments such as qEEG, EEG biofeedback, sound therapy and primitive reflexes are mainly delivered by registered psychologists in private practice. Psychologists are still not covered by Medicare despite continued efforts from their national body the Australian Psychological Society (APS) and increasing numbers of the public who are discontented with the quality of psychiatric care and the medical paradigm. Only a few of the more forward thinking private health funds cover psychologists and even then the amounts offered are usually tokens (eg. MBF pays $30 per visit with a total of $500 per member for a year!). This matter also requires investigation.

Assessments and Interventions

Implicit in the model offered here are assessment tools and therapeutic interventions which have had little prior application to learning difficulties and ADHD, but which may partly or wholly alleviate these conditions thus providing a management plan which offers much more than simply masking symptoms.

Since all learning and behaviour starts in the actual physical functioning of the brain, early intervention strategies must begin with the brain [16]. Unless the brain works correctly, you cannot learn adequately or be who you really want to be. "How your brain works determines how happy you are, how effective you feel, and how well you interact with others. Brain patterns help you (or hurt you) with your marriage, parenting skills, work and religious beliefs along with your experiences of pleasure and pain". And "normalising abnormal brain function can change people’s lives, even their very souls"[16] .

Therefore assessing brain function whenever learning or behavioural disorders are suspected is of paramount importance. Any assessment procedure, which does not take into account genetic, neurophysiological, metabolic and structural factors that contribute to brain functioning, will therefore be inadequate because it will fail to investigate the important underlying neurological conditions.

Quantitative Electroencephalography (QEEG)

Many psychiatrists and paediatricians involved in the diagnosis of learning disorders and ADHD are unaware of a significant body of research which supports the use of quantitative electroencephalograph (QEEG) analysis as a diagnostic tool for differentiating between organic and functional brain disorders including learning difficulties, ADHD, schizophrenia, epilepsy, cerebral atrophy associated with alcohol abuse, depression and anxiety [17-18, 47].

The QEEG is an objective and effective tool that uses digital technology to measure electrical patterns at the surface of the scalp which primarily reflect cortical activity or "brainwaves". A multi-electrode recording of brainwave activity is made under four conditions (eyes closed, eyes open, and during cognitive challenges such as reading and arithmetic) and converted into numbers by a computer. These numbers are then statistically analysed and compared to a database. Such comparisons allow the clinician to determine whether or not brain functioning is abnormal, to what degree, in what locations and in which frequency band. The procedure has the advantage of being non-invasive and requires no more than a few hours administration.

Neurologist John Hughes from the Department of Neurology, University of Illinois School of Medicine and psychiatrist E. Roy John from the Department of Psychiatry, New York University Medical Centre state in their 1999 paper on Conventional and Quantitative Electroencephalography:

"New three-dimensional QEEG imaging methods offer an economical alternative to other functional brain imaging modalities…..During the last decade more than 500 EEG and QEEG papers have reported well designed studies, concurring that EEG and QEEG abnormalities are found in a high proportion of psychiatric patients. Conditions such as anxiety disorder, depression, dementia, obsessive-compulsive disorder, schizophrenia, learning disabilities and attention deficit disorder with and without hyperactivity are now understood to involve interactions between brain dysfunctions or altered neuroanatomical structure and environmental influences. An overview of the findings reveals numerous consistent and concordant conventional EEG and QEEG findings among studies within the same DSM (III & IV) diagnoses"[47].

Hughes and John continue to say that the "independence of the normative QEEG descriptors from cultural and ethnic factors enables objective assessment of brain integrity in persons of any age, origin or background. This independence and specificity, as well as high replicability, has been established in studies from Barbados, China, Cuba, Germany, Holland, Japan, Korea, Mexico, Netherlands, Sweden, the United States and Venezuela. Such a high level of specificity is beyond the confidence level achieved by many routinely used clinical tests such as mammograms, cervical screenings or CT brain scans"[47].

Concerning Specific Learning Difficulties (SLD) and ADHD/ADD they acknowledge the considerable comorbidity between the two disorders and state that "precise and accurate determination of the presence of ADD/ADHD versus SLD can be of critical importance in avoiding the potentially devastating impact of these disorders on children and their families. EEG and QEEG can contribute usefully to this distinction, as well as to separating children with social or motivational factors underlying school problems from those with organic dysfunction" [47].

There is a wide consensus in the literature that children with SLD show a high incidence of excess theta or decreased alpha and/or beta activity with theta or alpha excess often seen in children with ADD or ADHD [48-59]. The types of QEEG abnormality found in SLD children relate to academic performance [60]. Hughes and John state: "a large percentage of children with attention deficit problems (more than 90%) show QEEG signs of cortical dysfunction, the majority displaying frontal theta or alpha excess, hypercoherence and a high incidence of abnormal interhemispheric asymmetry [59, 61]. Using QEEG measures, it has been possible to discriminate replicably ADD/ADHD versus normal children with a specificity of 88% and a sensitivity of 94% [62] and ADD versus SLD children with a sensitivity of 97% and a specificity of 84.2% [47,62].

As far as the use of medication is concerned they echo what other MDs (Breggin, Lyon, Hyman, et al) are saying and I quote: " Medications that profoundly alter the availability of neurotransmitters and affect a hypothesised pathophysiology are routinely prescribed by psychiatric practitioners. Nonetheless, little or no attempt is made in most cases, even in the treatment-resistant patient, to use biological assessment methods to select a treatment, to evaluate its physiological effect and to demonstrate its efficacy objectively[47].

Hughes and John conclude that "QEEG studies are particularly well suited to identifying subtle changes in the topographic distribution of background activity and can aid in difficult differential diagnoses such as assessing cognitive, attentional or developmental disorders" [47].

On a recent visit to Japan it was interesting to note the headline in the New Year’s Special of The Daily Yomiuri [87] which read "Have the Japanese changed?- Seeking a new path in the 21st Century - Young people suffer from immature frontal lobe" written by professor Toshiyuki Sawaguchi (brain science) of Hokkaido University. He begins his article by saying that he fears "that many young people today are mentally dysfunctional and unless measures are taken immediately, this country will be confronted with a serious situation this century"[p 5]. He continues to say that what is happening in Japan today appears to be completely different from what took place in the past. Young people he asserts, "seem to be completely indifferent to what other people might think of them….in class they unconcernedly munch on bread and answer mobile phones".

Sawaguchi asserts that those who suffer from frontal lobe dysfunction exhibit the same symptoms as young people today…. "They ignore situations or people around them, suddenly become upset in quiet gatherings, make obscene remarks, have an inability to understand other people’s feelings or restrain their passions, or they are unable to determine what their goal is in life or make efforts to achieve anything". This is because the frontal lobe plays a central role in controlling this behaviour" and Sawaguchi is extremely concerned about the escalating crimes and impulsive behaviours now being exhibited. He feels that environment, education and changes in dietary habits have contributed to the decline in frontal lobe functioning amongst Japanese youth. He calls for a return to traditional child rearing practices and dietary habits and for schools to "nurture the frontal lobe"[87]. Any professional (mental health, educational) or carer involved in the nurturing or education of a child with SLD or ADD will easily recognise these behaviour patterns.

Additionally, brain researchers are now beginning to explore the connection between addictions and ADHD[168-169]. Those with ADHD are also more likely to experience "reward deficiency syndrome" as their brains crave adequate levels of daily pleasure through simple daily activities. Thus those with ADHD are literally "sitting ducks for addictions".[10] In many instances , the only time a person with ADHD feels focused and satisfied is when they are "high"on drugs, alcohol, pornography or gambling. See Appendix E (p 54) for the relationship between marijuana and ADHD. Others chain smoke or drink their way through their stressful lives without consideration for the long-term consequences. Many choose to pursue high-risk activities such as gambling or sexual promiscuity, high-risk business ventures and dangerous sporting activities. Brain damage due to alcohol, marijuana, heroin, cocaine or prescription and illicit drugs is evidenced in SPECT studies[16] and in the QEEG. Therefore, it would be prudent to prohibit the leagalisation of marijuana.

Neurofeedback

The sister technology to QEEG analysis, neurofeedback (EEG biofeedback), is used to normalise aberrant activity. Neurofeedback is based on the research of Professor M. Barry Sterman of the UCLA School of Medicine, Departments of Neurobiology and Behavioural Psychiatry. He recognised that rhythmic EEG properties and brain function could be altered and normalised by operant conditioning of EEG patterns[18]. It is one of the fastest growing new modalities in the USA and now Australia, for addressing a variety of psychological, psychiatric, and neurological problems. Neurofeedback allows the therapist to address the physiological basis of behavioural problems with or without medication. Neurofeedback is a non-invasive, drug-free training modality which uses the principles of operant conditioning to teach the brain to self regulate.

There have been many outcome and controlled studies (See Appendix C pg 50) in peer reviewed journals attesting to the efficacy of neurofeedback. The entire January 2000 edition of Clinical Electroencephalography, a medical journal, was devoted to neurofeedback. The Neurology Editor, Frank Duffy MD who directs the Clinical Neurophysiology Laboratory and Developmental Neurophysiology, a research Laboratory at the Children’s Hospital, Boston, that is affiliated with the Harvard Medical School stated in his editorial:

"The literature which lacks any negative study of substance, suggests that Neurofeedback should play a major therapeutic role in many difficult areas. In my opinion if any medication had demonstrated such a wide spectrum of efficacy it would be universally accepted and widely used"[26].

In November 2000, it was reported that EEG biofeedback was being considered for approval by the National Institute of Mental Health in the USA as a preferred method of treatment for Attention Deficit Hyperactivity Disorder and epilepsy.

The committee is directed to the accompanying clinical paper "Assessment and Neurotherapy in the treatment of ADHD" written by Jacques Duff, a psychologist colleague in Melbourne. Interested readers are directed to the attached references listed in Appendix C (page 50) for studies on the efficacy of neurofeedback in the treatment of ADHD, LD and Epilepsy.

The use of QEEG evaluation and neurofeedback training in this clinic over the past five years has consistently produced results equal to that of overseas clinics[172] and other practices in Australia (currently there are about 20 practices nationwide). However, since these services are delivered mainly by psychologists and are not covered by Medicare and only covered by a few health funds, these interventions have been beyond the financial means of those most in need of evaluation, education and training. Furthermore, most general practitioners are unaware of their own literature and are reluctant to refer patients to psychologists in keeping with the accepted medical model (pharmacological paradigm) and also in fear of ridicule and/or reprisals from their psychiatrist colleagues.

The use of EEG biofeedback in public schools in America has been occurring for over four years. The Yonkers School District in New York, an extremely low socio-economic area, is but one district employing this powerful tool. Some of the continued benefits include less teacher absenteeism, less student truancy a decrease in aggressive and violent behaviour together with more positive academic and social outcomes for students with learning, attentional and behavioural disabilities. These positive outcomes have ensured that this method will remain in those schools.

Diet and Nutrition

From the Learning Pyramid Model it is also clear that the most fundamental intervention of all is to ensure that our children are fed "brain-healthy" foods. When dealing with learning and behavioural disorders it is foolish to underestimate the importance of basic biology to a person’s capacity to function "because we all have brains and our brains, like any other organ in our bodies, can be in better shape or worse. "The brain needs "care and feeding" too"[19].

Food is not just a source of energy; it is also a source of information for our bodies and as such can influence the neurochemistry of our brains. One of the most underestimated factors usually overlooked by the medical profession is the importance of biology to a person’s capacity to function in their social and educational worlds. Biology has profound effects upon a person’s psychology [19] and our biology is affected by the foods we eat and the chemicals in them. Children and adults with ADHD and comorbid disorders such as learning difficulties, dyspraxia, depression, anxiety, mood swings, obsessive compulsive disorder, epilepsy, Tourette’s Syndromme, Asperger’s, autism etc. are more sensitive to certain foods and the chemicals in them than their "normal" counterparts[20-21].

Mounting evidence indicates that the food we eat can cause or aggravate a variety of undesirable symptoms ranging from irritability, depression, mood swings, restlessness or inattentive behaviour, sleep disturbance, eczema, other itchy skin rashes, migraines, recurrent headaches, stomach discomfort, bloating, diarrhoea, reflux, colic and urinary infections to asthma, cancer and irritable bowel syndrome. Sue Dengate, food intolerance counsellor and author says, "Some people who are affected have never noticed a food reaction".[20]

Major changes in diet, food manufacturing processes and breast-feeding habits have resulted in a population totally out of line with our genetic imprint. Australian consumers have been too readily influenced by American dietary habits to the point of thinking "that bread and milk are quintessentially "natural foods"…however from the stand point of genetically determined human biology these foods are "Johnny-come-latelies", says Boyd Eaton, MD, Emory University [4], especially in the forms in which we consume them today.

Gluten/Dairy intolerance/sensitivity

Current research is consistently illustrating that gluten, a protein found in wheat, rye, barley and oats and casein a protein found in milk are powerful neurotoxins or exorphins. These exorphins are morphine-like peptides[23], which result from the partial digestion of foods and have repeatedly been implicated in investigations of ADHD[24]. These exogenous opioids (derived from external sources, instead of being synthesised within the body) have been shown to bind to the same cellular receptors that endogenous opioids bind to, thus impacting on the immune system, nerve function, myelination processes, vascular walls, neuromuscular function, and a variety of CNS functions[43]. The similarity between these exogenous, opioid-acting peptides and narcotics derived from opium, such as morphine, is suggested by similarities in function and attachment at identical receptors as well as by the blockage of such binding by drugs which also block the binding, at the same receptors, of opiates[23]. Opioids, in general, have been implicated in sleep onset[42] and hypothalmic-pituitary-adrenal axis function[43]. Reduced attention may be the result of the CNS attachment of opioid-acting exorphins because they behave like neurotransmitters[44]. As may be expected, such opioids can have an anaesthetizing, analgesic, and addictive effect.

Exorphins enter the blood stream when intestinal permeability is increased (which can result from the inflammation of the tissues that form the wall of the small intestine). There is a variety of possible causes for this such as auto-immune disease[63], yeast overgrowth [64], bacterial infections [65], ingestion of non-steroidal anti-inflammatory drugs [66], coeliac disease, milk protein intolerance, etc. Specific serum antibody production implies that macromolecules of partly digested dietary protein are being absorbed through the intestinal wall and into the bloodstream.

People with learning difficulties, specifically with reading problems, have been reported to have an increased individual and family incidence of immune problems and auto-immune disorders, particularly those involving the gastrointestinal tract and thyroid gland[67], which is relevant, given the very high comorbidity of ADHD and learning disabilities[68]. ADHD symptoms were also reported in association with an increased familial incidence of Crohn’s disease[67], which further supports the postulated connection. The reported excess of gastrointestinal malignancies among one group with learning disabilities, also becomes relevant[69], as does the excess incidence of malignancy, especially in the gastrointestinal tract and late onset diabetes, in untreated celiac disease[43]. As may be deduced from the above, there are many possible and probable causes of intestinal permeability. Undigested food particles are being absorbed into the blood of many apparently healthy people.

The exorphin hypothesis first postulated by Curtis Dohan suggests an interaction between a genetic predisposition and ingestion of two very common foods, dairy products and cereal grains containing gluten. He, and a team of health-care professionals, were the first to implement a clinical trial of a gluten-free, dairy-free dietary intervention as part of the treatment of schizophrenic patients that led to significant improvements[25]. Subsequent double-blind trials supported these findings[37-39]. There is a recent article suggesting an immunological connection between ADHD and schizophrenia[40]. It is also interesting that a report published in November of 1997 identified reduced perfusion (blood flow) of the frontal cortex, measured by photon emission computed tomography, in connection with schizophrenia. It is even more interesting that the patient in question was subsequently diagnosed with celiac disease, and following institution of a gluten-free diet, the psychiatric symptoms resolved and there was a normalization of blood flow to the frontal cortex[41].

Despite these findings over 30 years ago and a compelling body of direct and indirect evidence in the peer reviewed scientific and medical literature, as well as in anecdotal reports, which supports the exorphin hypothesis and its application to ADHD, it remains a relatively obscure perspective[43]. Dietary interventions in psychiatric conditions are not currently in vogue. Worse, proponents of such interventions are often mocked. The few orthomolecular psychiatrists in Australia who practice this intervention have been disowned by their own colleagues!

For instance, neither the medical interview nor the physical examination would be likely to identify coeliac disease. It is rarely considered, and physicians are rarely knowledgeable beyond the classic symptoms that apply only to a relatively small minority of untreated coeliac patients beyond infancy[70]. Coeliac disease is the most common food intolerance disease, suggesting that milk protein intolerance, and other such diseases would be even less likely to be identified by this process. An examination of dietary exorphins offers the possibility of a natural, long-term means to control symptoms and address the underlying causes for many who suffer from ADHD and learning difficulties. Testing of a random population sample in Iceland revealed that 15% of this group had elevated class G immunoglobulin (IgG) antibodies against gliadin, a group of proteins found in wheat[71]. The entry of gliadins into the circulation can apparently lead to tissue damage in most, if not all people. The genetic difference between health and disease may therefore be found in whether the mucosa can protect the individual from moderate quantities of gluten. Of course, hormonal and external factors may also affect intestinal permeability, thus further confounding an already complex issue. Evidence of exogenous peptides is frequently found, in a variety of mental illnesses including ADHD, schizophrenia, autism, in the characteristic patterns of excreted urinary peptides in each of these illness groups[37-41, 72-73].

Perhaps some of the most compelling evidence supporting the connection between the gluten/dairy connection and ADHD may be found in the study of patterns of electrical activity in the brain by Kittler & Baldwin[74] in 1970 and others[75-76]. This work showed improvement in ADHD subjects' EEG patterns, in response to diet and while they recognised that EEG patterns have long been known to be abnormal in some allergic children, they also believed that improvements of such EEG abnormalities had not previously been connected to dietary changes in those with learning problems. The EEG abnormalities in food-induced autoimmunity such as coeliac disease also has a surprisingly long history in Europe, although no reports of such work published in English can be found. In a translation from German, Paul et al. (1985) tell us that Sidor & Mitarb and Karczewska & Mitarb suspect this mechanism to be the direct effect of the gluten upon the central nervous system and hence on the brain wave curves[77], while Paul et al. have reported their own investigations using EEG, in addition to other techniques.

Their EEG investigations revealed that 38 of 58 (66%) of the coeliac children studied showed pathological EEG changes which increased with increased duration of gluten consumption, and that the long-term compliance with a gluten-free diet decreased the probability of pathological readings. They go on to provide evidence for a correlation between the extent of mucosal damage, and the duration of pathological EEG patterns and contend that the psychological signs in celiac children reflect a direct or indirect influence of gluten ingestion, and that damage to the intestinal mucosa is always accompanied by pathological brain waves in the celiac children studied. Several interpretations for this are:

  1. People with damaged small intestines absorb more toxic substance, resulting in the pathological changes, or;
  2. Toxic, gluten-derived proteins and peptides may cause the pathological changes;
  3. Both of the above dynamics contribute to the pathological changes[43].

Kozlowska[78] has reported a very similar incidence of EEG abnormalities in 71% of the coeliac children studied. She has identified these abnormalities as the same as those found in ADHD. Uhlig et al[79] reported their 1997 finding that topographic mapping patterns can be manipulated by changes to the diet among ADHD subjects. Refined sugar, milk, and gluten proteins were most frequently implicated in the ADHD-specific abnormalities identified in topographic EEG mapping The importance of this startling report from Uhlig is difficult to over-emphasise because it provides objective evidence for a connection between food intolerance and ADHD.

It is hoped that the work of Ulig et al. (1997) in demonstrating EEG changes associated with dietary factors among ADHD subjects will finally facilitate an end to such debates. Published replications of this group’s findings may finally induce pediatricians, teachers, and parents to engage in a careful search for dietary pathogens prior to leaping for easy pharmacological answers.

The complete and partial remissions reported in the literature leave little doubt that consumption of this common food group can result in functional and morphological changes to the central and peripheral nervous systems. It should therefore not be surprising that behavioural, mood and attentional changes also occur in response to these foods. In fact, the opposite would be surprising.

Food additives/chemicals

Health professionals have continually told us that only a minor percentage of the population is affected by food chemicals. This is incorrect. As many as 90% of the SLD,ADHD/ADD, mood and behaviourally disordered clients (children and adults) seen at this clinic show significant adverse reactions to common foods in the Australian diet.

Anyone can be affected if the dose is high enough, and over recent years the levels are becoming increasingly high. The common assumption that reactions to food are immediate is false. Most food reactions are delayed because they are not the classic allergic reactions as in Type I or II Hypersensitivities and therefore do not involve the immune system; rather they are due to side effects from food and the chemical additives (preservatives, flavour enhancers, artificial sweeteners and colours) in them.

Sue Dengate, food intolerance counsellor and author of "Fed Up", states that an estimated 15% of school children are so severely affected by adverse reactions to food that they are at risk for literacy and numeracy problems and that most health professionals emphasise medication and dismiss the role of food in disruptive behaviours. She goes on to say that "changes in behaviour and learning ability are the early signs of chemical toxicity, yet food chemicals are not tested for behavioural or learning effects before they are approved"[20].

Furthermore, Australia has failed to take notice of findings in overseas countries and still allows the use of preservatives & pesticides banned in other countries. An example of this is the preservative calcium propionate (282) found in commercially made bread (including gluten free bread. This preservative has been associated with migraines, skin rashes and non-cancerous tumours in rats. It has been banned in the UK. Apart from the gluten in bread, which is a potent neurotoxin (exorphin), commercially made bread in Australia is also whitened with phosphates. Phosphates can alter the pH (acidity/alkalinity) of the digestive tract. When this pH level is altered to become more alkaline lethargy, listlessness and inattention result. When it becomes too acidic, hyperactivity, impulsivity and anxiousness increase.

Apart from preservatives, artificial colours, flavours and sweeteners can also affect some individuals. Aspartame, the most widely used low-calorie sweetener in diet colas contains about 40% aspartate which is a known excitotoxin. A study in the British medical journal Lancet (1986), revealed that aspartate actually increased the appetite! Furthermore, it has been known to cause brain tumours in rats. A breakdown product from aspartame can interact with nitrogen to form nitrosurea-like molecules, which according to recent research is the most effective agent for producing brain tumours in experimental animals. It is estimated that 100 million people drink aspartame-sweetened drinks. Low sugar products such as yogurt, snacks, chewing gum, medicines and vitamins are also sweetened with aspartate[20].

While food colourings have an immediate effect on a child, the effect of preservatives is often delayed. Bread, carbonated soft drinks such as colas and lemonade are loaded with preservatives. Preservatives are worse than food colourings. Most preservatives are colourless, odourless, tasteless powders – often added to processed and take-away foods by the handful and not measured out. Therefore consumers have no way of knowing what is added or how much, unless they ask.

The literature is clear that at least some cases of ADHD, learning disorders and mood disorders are either food induced or exacerbated by the ingestion of certain foods and food chemicals [20-25, 37-44, 63-66, 69-81]. The only real issue under debate is the proportion of children whose diet is partially or totally responsible for their problems.

In the light of this knowledge, it remains to be seen what recommendations this committee makes with regards to regulating the myriad of fast food outlets predominantly in the lower socio-economic areas of Sydney, the processed food which pervades school and hospital canteens, the exorbitantly high price which is paid for unprocessed health food products, the enormous difficulty finding them, and regulating advertising and the amount and type of chemicals added to processed foods so that consumers with allergies can make informed and affordable choices. A list of food additives, which are known or suspected to cause adverse reactions and that need to be eliminated from processed foods is in Appendix D (page 53).

Nutritional Supplementation

In our modern society fresh food is a thing of the past. The so called fresh fruits and vegetables we buy today have little nutritional value because they are grown in nutrient-deficient soil, picked before they ripen naturally, genetically engineered, gassed, irradiated, artificially ripened and stored for days before we eat it. Therefore, the Australian diet (like that of many industralised nations) lacks the essential building blocks of functional foods vital to our health and well being and is a predominant factor in the dramatic increase in learning disorders [4].

Genetically Modified Foods
Furthermore, genetically modified foods are now becoming a serious threat to the health of our nation. Fiona Douglas, agricultural scientist, teacher and now freelance journalist, in her book "Genetically Modified Foods Guide"[88] points out that consumer interests are not part of the biotechnology industry since

(1) there are no laws controlling the industry with biotechnology conveniently watching itself, (2) the Genetic Manipulation Advisory Committee (GMAC) is filled with members who have a vested interest in ensuring huge financial investments provide profits, (3) the GMAC dismisses consumer concerns and keeps them ignorant by refusing to insist on truthful labelling of food products.

It is obvious from Douglas’ statements that the genetic engineering sector feel that allergy and cancer sufferers, women trying to fall pregnant and sick and healthy people alike are incapable of seeking information and making their own decisions. They must fear that if people knew which foods were genetically modified they would naturally avoid them. Consumers are herefore not given a choice about what they eat because they are not informed.

Douglas continues to say that this contempt for consumers by biotechnology is evident in their actions since they have continually

"(1) sought exemptions from the laws of supply and demand – the laws of a free economy

(2) denied consumers the right to know and thus

(3) denied people the right to make choices and finally

(4) sought to prosper through keeping the consumer ignorant".

Allergies are on the rise worldwide and every time scientists insert new genes (proteins) into foods they add potential allergens. A recent news report (17/1/01) stated an alarming increase in asthma in Australia with 2 out of 5 children being diagnosed. Japan recently reported a 30% increase in allergies. Many issues still need to be addressed and allergy sufferers need to be aware that genetically modified food poses an increased risk of a potential life threatening allergic response.

In May 1999 only 10% of the estimated 50 products for sale on the supermarket shelves were submitted to the Australia and New Zealand Food Administration (ANZFA) for approval. Instead of prosecuting the tardy manufacturers, the ANZFA chose to water down its standards and it was now sufficient that the producers had merely applied for assessment. Their back flip, says Douglas, was supposedly to "avoid chaos in supermarkets if retailers were required to remove unlawful products from sale"[88]. Thus in ANZFA, the biotech industry had found an ally". It will now be at least another year before food safety laws are introduced.

As it currently stands allergy sufferers are not able to identify these foods since they are not required to be labelled and carry no warning. It would appear that the food industry are following their medical counterparts by keeping consumers ignorant and using methods that are far from scientific - all in the name of commercial success – worshiping the twin gods of commercialism and consumerism.

Given the discussion on food sensitivities presented in this paper, it is imperative that we stop assaulting our nervous systems with toxins and this is a matter that cannot be ignored by this committee. It requires urgent and direct attention and re-education at all levels of societal structure or we will continue to be faced with epidemic proportions of dysfunctional people and our jails will continue to swell. Failure to act on this will result in repercussions in every area of life- academic, social, emotional, employment and productivity. The health of a nation, and indeed the whole world, depends on ensuring that one of our most basic needs- food - is unadulterated and nutritious.

Essential Fatty Acid (EFA) Supplementation

Essential fatty acids such as linoleic acid (LA) and alpha- linoleic acid (ALA) are essential for life, cannot be produced by the body and must come from the food we eat. Since the body cannot make ALA from AA and vice versa, both these EFA’s must come from the food we eat. LA (omega 6) is found in seed oils such as sunflower, safflower, corn and sesame. ALA (omega 3) is found in dark leafy vegetables, flaxseed oil and rapeseed oil. These need to be converted by a series of enzymatic reactions to longer chain fatty acids to fulfill vital functions in the body. Three of the more important long chain polyunsaturated fatty acids (LCPs) are arachidonic acid (AdrA) which is produced from LA and then converted into eicosapentaenoic acid (EPA) which is then converted to docosahexaenocacid (DHA). The conversion process can be slowed by lifestyle factors including the typical Australian diet rich in hydrogenated and trans fatty acids in manufactured foods, stress, viral infections, alcohol and various illnesses

There is a greater percentage of fat in the brain than in any other organ and half of this fat is LCPs. DHA (omega 3) is the most abundant LCP in the brain with AA and Adr A the most abundant omega-6 LCPs. In his review of the scientific literature, David Horrobin[84], one of the world experts in EFA metabolism, has identified the chromosomes and some of the locations of genes for ADHD, dyslexia and verbal dyspraxia (apraxia) and he and his colleague Crispin Bennet have linked some of these locations with specific enzymes. The enzymes (Fatty acid-CoA transferase, Fatty acid-CoA ligase, Phospholipase C) are variously involved with fatty acid and membrane metabolism. Enzymes called transferase and ligase are associated with the incorporation of fatty acids into membranes, whereas the phospholipases are associated with the breakdown of phospholipid membranes.

Overwhelming evidence from the United States [89-90], Europe and elsewhere points to the need for the brain to be nourished with long chain polyunsaturated fatty acids (LCPs). One of the key problems that children with ADHD, dyslexia and dyspraxia appear to have is converting the essential fatty acids LA and ALA into the effective longer chain derivatives. Supplementation in children with learning disabilities and ADHD has resulted in a remarkable reduction and improvement in symptoms [89-100, 104].

In a landmark study at Purdue University, Laura Stevens et al [89] compared 53 ADHD boys between the ages of six and twelve to 43 non-ADHD counterparts. Their results published in the American Journal of Clinical Nutrition in 1995 demonstrated that the ADHD children

  1. displayed clinical signs of LCP deficiency such as excessive thirst and frequent urination,
  2. consumed plenty of LA and ALA precursors in their diet but had much lower levels of AA and DHA in their red blood cell membranes and higher levels of omega-6 DPA in the membranes. This indicates difficulty with converting LA and ALA into the long-chain derivatives AA and DHA.

They also found that the ADHD boys were less likely to have been breast-fed and were more likely to suffer from asthma and other health problems.

The Purdue researchers further investigated the behaviour, learning and health problems of the boys they had studied[90]. They divided the group of one hundred boys (aged between six and twelve) into those with high and low levels of omega-3 fatty acids in the blood. Results of this study were published in the medical journal Physiology and Behaviour in 1996 and showed that the boys with low levels of omega-3 fatty acids (1) reported significantly greater frequency of symptoms associated with LCP deficiencies including increased thirst, frequent urination and dry skin, (2) displayed significantly greater behavioural problems with more frequent and excessive temper tantrums, (3) had greater difficulty falling asleep and getting up in the morning, (4) demonstrated greater learning problems with teachers reporting overall lower academic ability and poorer maths ability. The researchers concluded that "these results, together with other previous descriptive studies, support a relationship between omega-3 fatty acid status and behaviour in children that parallels what has been reported with rats and monkeys" [90].

A group of Japanese researchers at the Toyama Medical and Pharmaceutical University[91] conducted a placebo-controlled, double blind study with forty-one male and female students who were given DHA or placebo capsules for three months before the beginning of their final exams. Those students who received the DHA capsules showed significantly less aggression during this stressful period than their counterparts who had received placebo capsules (no supplementation).

Whilst American researchers[89. 90, 92, 95, 100,103,104] were exploring the ADHD connection to fatty acids, Swedish[8-9] and British researchers such as Richardson[96, 101], Broadhurst [106] and Stordy [97-99] were exploring the connection between fatty acids and dyslexia and dyspraxia.

In addition to their American counterparts, British researchers found that

(1) mothers of dyslexic children had, while pregnant, been on a diet low in omega-3 fatty acids,

(2) young adult dyslexics had poor night vision and when supplemented with DHA (fish oil) daily for one month their ability to see in the dark became the same as that of non-dyslexics,

(3) when dyspraxic children were supplemented with DHA and evening primrose oil they showed significant improvements in a whole battery of tests as well as behaviour[4, 96-99.100].

Mothers need to be educated and encouraged to breast feed their babies for as long as possible as colostrum in mother’s milk is essential for brain development. Thus supplementing the diet of pregnant and lactating mothers with essential fatty acids, glyconutrients and amino acids supports optimum brain functioning in their offspring as well as themselves, and protects both from depression.

Horwood & Ferguson[82] recommend the need to "develop improved infant formulas with properties more similar to those of human breast milk that may lead to improved developmental outcomes in children". Stordy feels this is the crux of the problem since DHA which is a major constituent of breast milk, is not always found in manufactured formula. Frank Oski, MD, former chairman of pediatrics at the John Hopkins University School of Medicine says that because formula-fed babies in the United States "are deprived of this essential building block" there are "incalculable quality-of-life issues"[83]. He continues to say that studies[84] indicate that "for every year of delay, more than two million formula-fed full-term babies born annually in the United States may experience a disadvantage of three to six IQ points compared with breast-fed full-term babies". The difference adds Professor Oski, is even greater for infants with low birth weight[83, 102-104].

Broadhurst, Cunnane and Crawford (1998) state that "long- chain polyunsaturated fatty acid deficiency at any stage of fetal and/or infant development can result in irreversible failure to accomplish specific components of brain growth. There is good evidence today that lack of abundant, balanced DHA and AA in utero and infancy leads to lower intelligence quotient and visual acuity and in the longer term contributes to clinical depression and attention deficit hyperactivity disorder"[106].

Neutraceuticals

In addition to fatty acid supplementation the body also requires "functional foods" or "neutraceuticals". These are "foods that are thought to prevent disease" (Harvard Health Letter April '95). The building blocks of functional foods are called phytochemicals (plant chemicals) These phytochemicals (carbohydrates) are naturally occurring bioactive substances that prevent diseases by interacting with the body's innate healing process to maintain vibrant health and energy. These are only found in food that is ripened on the vine/tree and remain active for 48 hours after being picked. Without functional foods the body cannot continue the miracle of healing itself as these foods provide the raw materials needed to assist in this healing process thus giving the body fuel to perform at optimum levels.

Without sufficient functional foods the following four problems exist for all of us but most particularly for our children:

  1. Starvation: since most of our food is nutritionally deficient;
  2. Toxicity: many food products including raw fruits and vegetables contain toxins (pesticides, heavy metals) not to mention the air we breathe and the water we drink (contaminated by bacteria and purified with aluminium sulphate) which actually work against our body's natural healing process;
  3. Stress: as a result of malnutrition and high levels of toxicity; and
  4. Degenerative disease: which can be symptomatic of nutritional deficiency and as a result of stress on the body.

Of the 200 simple sugars (glyconutrients) occurring in plants, only eight are known to be essential for cell-to-cell communication. However, only two of these, glucose & galactose are found in modern diets. The body can convert these two into the six missing sugars, but this enzymatic process is long (up to 20 steps), unreliable and error-prone. Thus we all need to supplement our diets with these missing sugars.

All cell surface receptors, binding and signalling components are glycoproteins (proteins and sugar). They essentially act as the language between the cells in our bodies. If the correct sugar is not placed in the proper location or is missing, the glycoprotein is not formed correctly and will be unable to carry out its function in the cell membrane. Only effective cell membrane communication can make the correct cells for our organs.

It has been shown[107] that functional components of glyconutrients boost the production or activity of enzymes that act as (1) blocking agents (detoxifying carcinogens or keeping them from reaching or penetrating cells and (2) as suppressing agents (restraining malignant changes in cells that have been exposed to carcinogens). As such they can benefit those who have a decreased function of the immune system or increased oxidative stress; those with diminished/faulty neurotransmitter function or those with poor/faulty cellular repair capabilities. It has been demonstrated that when children with ADHD are supplemented with these glyconutrients many improvements in symptoms are seen[107-112].

Vitamins

Iron, magnesium, zinc, calcium, chromium and selenium have all been shown to be important for optimum brain function [10, 111]. Iron deficiency can lead to significant cognitive and behavioural problems in children. Magnesium has several important functions including a calming effect on nerves and muscles thus diminishing stress. It is also an important cofactor in the enzyme delta 6 desaturase that is needed for the conversion of vegetable derived omega-3 into the brain-critical fatty acid DHA. Zinc is also involved in many enzymatic reactions in the body. Low zinc levels result in a weakened immune system response and diminished digestive system function. Thus these children often suffer from coughs and colds, upper respiratory tract infections and stomachaches. It is also needed to help the body excrete toxic metals. Chromium is necessary in the regulation of blood sugar levels and many children seen at this clinic suffer from hypoglycemia that exacerbates their already difficult temperaments. Calcium plays important roles in the formation of bones and teeth, the clotting of blood, muscle contraction, nerve conduction and enzyme activity. If children are on dairy free diets, then calcium citrate supplementation is essential. Most children seen at this clinic will need some form of supplementation as well as being on a gluten-free and diary-free diet. When they break the diet or fail to take the necessary supplementation, their EEG patterns and behaviour alter dramatically.

Water

The simplest intervention for children with learning disabilities and ADHD is to ensure they get an adequate supply of fresh, clean water. Chronic low-grade dehydration may be one of the most widespread health risks all of us face. A dehydrated brain leads to confusion, irritability, malaise, cognitive problems, lethargy or hyperactive behaviour. Fatty acid deficiencies and food allergies can lead to excessive thirst and excessive urination and may be reasons why some children drink copious amounts of water and wet the bed. If the loss of fluids through the kidneys is not replaced these children can quickly become dehydrated. Unfortunately, Sydney water is far from the perfect beverage since the chemicals used to treat the water are themselves toxic and tap water contains many micro-organisms. Therefore, adequate filtration methods at home or buying filtered water becomes a necessity for these children and adds to the financial burden on parents.

Parent and teacher education, maternal health during pregnancy, neonatal care, diet and nutrition are the cornerstones to optimum brain functioning. Education in this regard needs to be totally restructured at every level and food producers/outlets must be made to comply with the Safety Foods Act fully disclosing the ingredients on all processed and take away food products. Genetically modified foods, artificial preservatives, colourings and flavours, yeast, MSG, hydrolysed fats and hidden sources of gluten all need to be clearly labeled so that consumers do not remain ignorant of what they eat and have the choice to avoid those foods known to provoke or exacerbate potentially serious allergic reactions. The elimination of the plethora of junk food available at school canteens and elsewhere also warrants action.

The exponential rise in the number of children with SLD and ADD/ADHD is alarming. Older members of the committee will remember when life was simpler, more basic and down to earth.

Fifty years ago, children drank water and cordial and soft drinks were considered treats for special occasions such as birthdays or Christmas, not consumed in vast quantities on a daily basis. The myriad junk snacks available today had not even been invented. Biscuits and cakes were considered rare treats. Homegrown fruit and vegetables were eaten, milk was not homogenised and bread did not contain the additives that it does today. Cattle and poultry were not pumped full of steroids and food had a natural flavour. Cotton was not treated with pentachlorophenol (PCP) pesticides containing dioxin a potent neurotoxin. There were less cars on the road, they moved more slowly than they do today and there was little or no smog. Walking, or riding a bicycle was the norm and our soil and water were not polluted with pesticides, heavy metals and virulent micro-organisms. Neither were we exposed to the myriad sources of electromagnetic radiation such as TV, computers, mobile phones and microwaves.

Once accurate assessment of brain functioning (QEEG which specifies brain wave patterns and differentiates between SLD and ADHD and other psychiatric conditions) has been conducted and the underlying medical conditions (allergies, food sensitivities, level of fatty acids in the blood, antigliadin antibodies, urinary peptides) are addressed through diet, nutrition and neurofeedback then assessments and interventions for other learning disorders such as central auditory processing, literacy and numeracy skills can begin.

Interventions for Literacy Skills

The next level of the Learning Pyramid requires the examination and remediation of the functional attributes of the central nervous system (CNS) which include the auditory and visual processing systems, motor coordination/balance and the vestibular system. Space precludes the discussion of all the interventions required here so only those interventions which are employed at this clinic will be addressed here. The reader is referred back to the model on page 13 the other relevant and effective interventions.

Central Auditory Processing Disorder (CAPD)

The importance of the auditory system in learning cannot be overemphasised. It is the only sensory system that is normally fully developed at birth and is closely related to vision and movement – all of which are crucial factors in the learning process. Thus it is important to ensure that this system is functioning well, early in the intervention process.

Central Auditory Processing Disorder (CAPD) is a subtle and often undetected disorder which is at the crux of most literacy difficulties and the most common deficit found in individuals with dyslexia and ADD/ADHD. CAPD is a deficit in processing information from audible signals not attributable to impaired peripheral hearing sensitivity or intellectual impairment. Thus children with CAPD are not deaf or mentally retarded but they have significant difficulty with the ongoing transmission, analysis, organisation, transformation, elaboration, storage, retrieval and use of information contained in auditory signals[112]. This deficit in the perception or complete analysis of auditory information is due to CNS dysfunction, usually at the level of the cerebral cortex.

According to the American Speech and Hearing Association (ASHA) Task Force on CAPD in 1996

"Central auditory processes are mechanisms and processes responsible for the following behaviours: (1) sound localisation and lateralisation, (2) auditory discrimination, (3) auditory pattern recognition, (4) temporal (time) aspects of audition which include resolution, masking, integration and ordering, (5) auditory performance with degraded acoustic signals and (6) auditory performance with competing acoustic signals"[113].

The process also "involves attention to detection and identification of the signal and decoding of the neural message"[114]. Therefore the way in which the CNS receives, perceives, decodes and utilises speech/sound signals is fundamental for the emergence of phonemic awareness and in the broader sense phonological awareness which are the foundation blocks to literacy[112].

Phonemic awareness refers to the ability to explicitly separate and manipulate the separate sounds in words. Phonemic awareness is not the same as phonemic discrimination. A child who can choose the correct picture when asked to distinguish between the spoken words boy and toy can obviously discriminate the sounds b and t, but may not be sufficiently aware of the separate phonemes to be able to point to the picture whose name starts with b, or say that there are two sounds in boy. Thus, phonemic awareness refers to the ability to consciously attend to a word's separate phonemes. Phonemic segmentation ability is not acquired naturally in the absence of an alphabetic writing system[115-116].

Phonological awareness is the ability to retain auditory information and distinguish the identity, number and sequence of sounds in words and is the most potent predictor of reading success or failure than any other previously examined factors[117-122].

The fact that phonemic awareness is causally related to reading acquisition has been further confirmed by demonstrations that children trained in tasks designed to induce phonemic awareness improve their reading skills more than children given no training[122-129] . Further, the relationship between phonemic knowledge and learning to read is reciprocal [130-131].

Whenever there is a history of recurrent middle ear infections (glue ear etc.) CAPD assessment is vital. For each ear infection, hearing acuity is likely to be reduced for up to six to eight weeks, after the acute stage of the infection has passed. What goes into the brain to become the language store (the way sounds, words and sentences are organised) is thus likely to be incomplete and inaccurate.

When CAPD is not detected or appropriately addressed children usually behave as if peripheral hearing loss is present, even though hearing sensitivity is normal. They may refuse to participate in classroom discussions or may respond inappropriately to questions or in peer conversations. Other common characteristics may include

Unfortunately, many children with CAPD are incorrectly diagnosed with ADHD/ADD and inappropriately treated with stimulant medication because the concept of CAPD is often difficult for parents, educators and medical practitioners to understand. It is thus rarely suspected or assessed. The problem becomes increasingly apparent once children start school and have to cope with poor listening environments such as open classrooms and background noise.

It is not enough to have a child’s hearing assessed by conventional audiograms since only four points on the hearing scale are tested and hearing is considered to be fine for language acquisition if it is in the range of 20-40 decibels. However, as the late Dr. Mary Lou Sheil (paediatrician in Sydney) so cogently pointed out, this standard was set for adults over 100 years ago when Edison and Bell’s invention – the telephone- became popular. "It has absolutely NOTHING to do with the ranges needed for a CHILD to be able to PICK UP and DISCRIMINATE the sounds of language in the early years of life when language is being laid down in the brain. Ranges needed for this difficult task are more sensitive"[132].

Alfred Tomatis, a French ENT surgeon and the father of modern sound therapy, demonstrated that in order for infants and young children to lay down the sounds of the English language they need to hear up to 8,000 Hz at minus 10 decibels. For instance, to hear the sound "th" in the English language requires hearing to be at minus 5 to minus 10 decibels and in the range of 6-8,000 Hz.. We are all born with this ability but as we listen to the sounds of our native language, our ears gradually close to frequencies not needed in our mother tongue. By the age of seven years, this process is complete and explains why younger children speak a new language better than their older siblings and parents[133].

The SLD/ADHD children tested at this clinic are assessed for the full range of both frequency and loudness and it has been found that over 80% of them are not hearing with enough sensitivity. Furthermore, effective auditory and visual processing requires a speed of 100msecs. Children tested at this clinic invariably have processing speeds slower than 400 msecs and some as slow as 700 msecs. Additionally, a significant number with severe behavioural and emotional problems are either left ear dominant or exhibit no clear dominance of the right ear. Right ear dominance is essential for the fast and efficient processing of sound as the language centre, which processes auditory information is in the left hemisphere of the brain in 97% of right handed people and 70% of left handed people. Auditory information which travels predominantly via the left ear will therefore arrive at the auditory cortex later and more weakly than that which travels via the right ear as it has further to travel[134].

Galiaburda et al[135], Livingstone[136] and Lovegrove[137] have demonstrated that there are specific nerve pathways in the auditory system which respond to the onset and offset of a tone and to the increase or decrease in frequency. These two pathways are (1) the magnocellular or large cell pathway and the parvocellular or small cell pathway. The magnocellular or transient pathway relays the onset and offset (fast changing) stimuli in speech and music as well as changes in localisation of sound , and changes in figure ground noise. This pathway is also involved in sensory motor feedback loops. The parvocellular or sustained pathway relays slow/non changing stimuli such as long tones and stable background noise and emotional content. It has been shown that it is the magnocellular pathways that function poorly in the LD/ADHD child[135-137]. Moreover, Talall et al [138] has found that it is the right ear, which picks up the very fast changing consonant sounds and sends them to the left brain for processing.

While the NSW Department of Education acknowledged in their support document of 1992[139] that auditory perception difficulties are the most common problems evidenced in children experiencing difficulties in reading and writing, it has failed to realise that it is a neurological deficit. Most classroom teachers and support teachers are unaware of the existence of this document or that CAPD is a neurologically based deficit and that unless it is adequately addressed a third of children will continue to struggle with acquiring basic literacy skills despite receiving remedial help in reading and spelling. School counsellors do not have the training or tools to detect CAPD and are content to accept a normal result of hearing acuity. But as previously discussed a normal result on a conventional audiogram is meaningless in terms of speech and language acquisition. Furthermore, the few school counsellors who are aware of the work carried out by this and other clinics like it in Sydney, are prohibited from referring children in need of assessment and treatment thus denying these children the right to learn and a better quality of life.

SAMONAS Sound Therapy (SST)

SAMONAS sound therapy developed by Ingo Steinbach[143], a German sound engineer, physicist and musician, is based on the work of Dr Alfred Tomatis. It addresses CAPD by providing extra stimulation to the brain so that auditory, visual, motor and other associated neural pathways are established or modified. The full range of frequencies is specially recorded and spectrally activated. The specially filtered music, that contains sudden bursts of high, harmonic sound, stimulates the onset/offset mechanism in the magnocellular pathways in the brain. Through air and bone conduction this stimulation increases auditory and visual processing speed. Perception of sound, of proprioception and the vestibular system is sharpened. Since sound enters the midbrain so low down it is postulated that the entire sensory system is enhanced. SST also helps to integrate the functioning of the magnocellular and parvocellular pathways as well as the right and left hemispheres in the brain. It also develops dominance of the right ear because some of the classical music on the compact discs is louder in the right ear by as much as 6-8 decibels.

It has been the experience of this clinic and other practitioners in Australian that when SAMONAS Sound Therapy is done prior to remedial programs it significantly reduces the intensive time and individual effort required from all parties concerned. In some cases it resolves literacy skills to the extent that remediation is no longer necessary. SST can and has been done in clinic settings with bone conduction, at home and in classrooms under the supervision of an experienced and qualified therapist.

It is interesting to note that a recent television segment on "Today Tonight" (Monday 8/1/01) highlighted the auditory processing deficits in boys compared to girls of the same age. Ron Whittaker of the National Acoustics Laboratory (Sydney) found that boys’ hearing is deteriorating and diminishing to the extent that a ten year old boy can only hear and process auditory information as efficiently as a twenty-five year old man. One can only speculate as to the causes of this alarming finding. Possible contributors include loud stereos, music that mainly consists of low frequency sounds, doing homework with headphones on or with the television blaring in the background. Boys are at greater risk of reading and literacy failure and since CAPD is seldom detected and assessed by teachers, school counsellors and paediatricians it is important that these personnel be educated in this area and with more than just a few snippets on television.

Lindamood Auditory Discrimination in Depth Program (LADD)

As mentioned earlier, phonological awareness (the ability to retain auditory information and distinguish the identity, number, and sequence of sounds in words) has proved to be the best predictor of reading success or failure. The Lindamoods maintain that 85% of learning disabled children have an inability to remember what they hear and they refer to this as an incompletely developed auditory conceptual function. This neurological deficit occurs randomly in 33% of the population and is independent of race, sex, intelligence and cultural factors such as education and socio-economic status[128].

The LADD program is a multisensory preparatory program that develops the auditory perceptual skills basic to reading, spelling and speech and is complementary to any reading program. It begins at a level prior to that at which most phonics or reading programs generally begin. Thus it is ideally suited to teaching children from kindergarten through to Grade 2. The auditory elements of speech and sound are linked to the basic oral-motor activity that produces them. Through discovery and manipulative activities children are gradually led through a series of small steps which ensure success and leads to the development of sound-symbol association to spell (encode) and read (decode) single as well as multi-syllable words. Thus the child’s ability to consciously monitor sensory cues from the ear, eye and mouth helps the child to make perceptual judgments necessary to perform at an automatic, self-generating, self correcting level of response in reading and spelling tasks and in speech.

Longitudinal studies (Idaho School Disctict 1974, Santa Maria Eelementary School District California during 1983-85, Reading Foundation, Calgary Canada, 1990) have reported the success of this program with Kindergarten to second grade students as well as with reading disabled individuals[144]. In my role as a District School Counsellor, I conducted a pilot study of this program in 1988. The results confirmed a statistically significant improvement in reading and spelling with children across various grades. Unfortunately bureaucratic red tape prevented the publication of these results.

I have used this program extensively over the last 12 years in government and private schools, and in this practice with children and adults of varying functional and age levels and ethnic backgrounds, and have trained others (teachers, speech therapists, psychologists, parents) in its use. The LADD program is available commercially and there is the temptation to simply "buy the kit" and use "bits and pieces" from it. This action is strongly advised against for three reasons. Firstly, extensive training is required if the program is to be taught effectively; secondly, since it is an American program it needs to be adapted for Australian pronunciation and thirdly, a third of all teachers themselves will have the same problems they are trying to prevent and remediate in their students.

The complementary program for teaching critical thinking and higher order comprehension skills is Nanci Bell’s Visualising and Verbalising (V/V) program[170]. This program develops the process of visual or concept imagery that is the basic to reading comprehension, receptive and expressive language and written expression. The imaging process moves from small units of language (words) to the larger units (sentences, paragraphs, pages, chapters). Verbalising information requires the organisation of language and the imposition of a logical structure. Visualising incoming information allows us to remember information in a sequence and see how different parts relate to each other. The V/V process is very powerful. Once developed it allows the individual to (1) image parts and process them into wholes or "gestalts" so that they get "the bigger picture" and not just a few isolated details, (2) recall and relate the imaged gestalts, and (3) reorganise and verbalise concepts, using the imaged gestalts as a reasoning foundation. Comprehension is in essence, critical thinking. It requires the ability to recall, relate and reorganise. It is the ability to relate new information to one’s previous knowledge and experience. Therefore comprehension and critical thinking are a generative process with imagery as the foundation and sensory connector.

Consistent results during the past 12 years has convinced me that the Lindamood-Bell program is unparalleled in its ability to deliver the gift of reading and comprehension to those who have struggled for years and failed with other methods. Multi-sensory methods such as the Lindamood and Bell programs "are par excellance tools for forging links between these things"[124]. In the hands of trained and experienced professionals, this is a powerful preventative, instructional and remedial tool, surpassing by far outcomes achieved through Reading Recovery and Spalding simply because it does not assume adequate auditory perceptual skills and visualising ability but develops them as part of highly structured yet flexible programs.

Any literacy program that assumes adequate auditory processing skills, ignores the phonological processing difficulties experienced by students with learning difficulties or fails to teach metacognitive strategies such as visual imagery, will be ineffective in developing independent, self-correcting and self-monitoring readers and spellers.

Primitive Reflexes

An assessment of neurological functioning would not be complete without a look at the status of a child’s primitive reflexes. Primitive reflexes are automatic, stereotyped movements directed by the brain stem and executed without involvement of the cortex. They are essentially survival reflexes that occur sequentially in the first few weeks of foetal development. They should only have a limited life span and then be inhibited or controlled by the cortex to allow more sophisticated structures (the postural or adult reflexes) to develop, and to take control of voluntary, directed responses.

For a variety of reasons, primitive reflexes are sometimes not transformed into postural reflexes and they remain active beyond the first 12 months of life. These aberrant reflexes are evidence of a structural weakness or immaturity within the CNS. Their prolonged presence impedes subsequent motor control, sensory perception, eye-hand coordination and cognition[140-142, 171]. Symptoms of neurodevelopmental delay range from clumsiness and ambidexterity, to learning difficulties and emotional disorders.

In a recent study in a primary school in Sydney (1999) as many as 48% of kindergarten children were identified by myself. A week later, student occupational therapists identified the same children. Since no therapy was forthcoming, the school invited me to initiate the Primitive Reflex Program. This program is based on the principle of replication and brain plasticity. By replicating specific stages of development through the repetition of movement patterns based upon early development, the brain is given a "second chance" to establish neural connections and reset the "neural clock" to the correct time. The exercises were designed by Blythe and Goddard of the Institute for Neuro-physiological Psychology in Chester, England based on the work of Swedish researchers Johanneson-Alvegard and Kjeld Johansen[142].

At the end of a year, those children who completed the program had virtually no primitive reflexes remaining and had made significant gains in social and academic areas. It must be pointed out that occupational therapy programs that target the improvement of specific skills without addressing the underlying retained primitive reflexes have at best, a limited chance of success. This is reflected in the fact that most children who attend this clinic have been in such programs for years and their handwriting remains laborious, immature or almost illegible.

Discussion on the Impact of Learning Difficulties

Learning Disabilities and ADHD are lifelong and pervasive. They affect academic, social and family life, self- esteem and employment opportunities. The stress learning disabled children experience leaves them feeling tired, unmotivated and overwhelmed.

Academic success for LD children often depends on two vital factors

(1) the acquisition of literacy and numeracy skills at a level that will enable them to access information efficiently and express themselves in the written form and

(2) the preservation of self-esteem, motivation and confidence.

Many LD children who fail daily in academic settings understandably develop avoidance strategies. School phobia, truancy, aggressive and disruptive behaviour, withdrawn detachment, the creation of fantasy worlds, limitation of expectations and "dropping out" are all strategies to relieve anxiety and stress.

It is not uncommon for these children to get stressed when they have failed and people say, "Never mind, -you did your best". They don't want to fail when they know they have done their best. Therefore, if they think they are going to fail then they won't do their best so when they do fail they can think, "Well, I didn't try". It is important to remember that "there is no positive reinforcement more effective than success" (Frostig & Maslow[173]).

Since literacy and numeracy skills dominate the school day at every level of education, attention to these is vital as early as possible. These children know they have to work harder than their peers do in order to reach their potential. The enormous effort required of them has to be experienced to be appreciated. Homework is tedious as the amount of time to complete assignments is usually ten times as long as for normal children.

"If it takes around 100 hours for a normal child' to master a skill, it takes a LD child 1000 hours to reach the same level" (Fawcett[174]). It gets even worse as the number of hours for a normal child to learn a skill increases!

Therefore strategies and skills must be taught and practiced early if they are to become automatic and lay the foundations for the work that underpins the more formal secondary curriculum. "Unless basic skills are taught before the child reaches secondary school, the gap between his level of ability and that of his peers will have widened to the extent that catching up will be an almost impossibly long and demoralising process" (Thomson[175]). Failure to acquire these skills usually leaves brighter children more inclined to adverse emotional reactions, which further blocks their capacity to learn. The inability to capitalise on potential, to express ideas concisely, tell inventive stories plausibly, or to communicate original concepts is a major source of stress.

Every child has the right to learn no matter how different they are. Every child has the ability to learn - we just need to find the right keys. These keys include accurate early identification, interventions that do not harm the child; an educational environment that nurtures the frontal lobes and an encouraging and supportive teacher well versed in the diagnostic tools and intervention methods outlined in this paper. Teachers who can mediate with professionals and communicate concerns and suggest appropriate choices to parents are invaluable in the life of learning disabled children. Teachers who continue to "pound away" at teaching strategies that have failed in the past (because they were inappropriate for the child’s needs), are guilty of what Saunder's terms "academic abuse"[176]. It shows poor judgement and is a waste of student and teacher time. Schools that are aware of the difficulties but fail to adapt to accommodate these students are also guilty as "diagnosis without treatment is criminal"( Margaret Rawson (Past editor Emeritus of Annals of Dyslexia and council advisor, published by the International Dyslexia Association)[177].

Effective early intervention will reduce the number of offenders coming before the criminal justice system as persons with ADHD and learning difficulties statistically interact more frequently with the criminal justice system compared with normal individuals[182-83]. Of the hyperactive and impulsive group approximately 50% will progress to a level of aggressive behaviour defined by most law enforcement agencies as delinquency according to the FBI Law Enforcement Bulletin[182]. This makes the need for early intervention even more crucial.

As we are all aware, children value themselves to the degree that they have been valued. A positive identity hinges on positive life experiences. "The key to inner-peace and happy living is high self- esteem, for it lies behind successful involvement with others" (Briggs[178]). Society as it is presently structured does not support these children or their parents, at any level.

Recommendations

As discussed in this paper Learning Difficulties (including ADHD) and associated comorbidities are lifelong disabilities and will require adequate and effective ongoing multi-modal management and support. Thus early intervention must target not only the learning disabilities and attentional deficits but also the comorbidities. In keeping with the Learning Pyramid Model (p13) and the Model of Functional Medicine (page 14), the following recommendations are made.

Interviews and Assessments

  1. Parent Interview – A diagnostic interview is conducted with the parents and the compilation of a great deal of data, taking into consideration the child’s social, school, and family situation, developmental status, and a host of other factors is followed by a brief interview with the child. Teacher questionnaires reporting on the child’s behaviour also need to be considered at this stage.
  2. Medical Interview - A medical examination of the child which does not merely measure weight, height, blood pressure or head circumference but one that takes into account the full family medical history and presenting symptoms of the child. As a result several of the following diagnostic tests may be necessary: full iron studies (ie. Ferroxin stores as well as levels), liver and thyroid function tests, blood fatty acid analysis, urinary peptide analysis, faecal stool analysis, hair analysis (for nutrient status as well as heavy metal poisoning), ELISA testing for food allergies which detects both IgE and IgG antibodies formed against food antigens with a high degree of accuracy (conventional RAST testing is not sufficient).
  3. Nutritional Assessment - Referral to a nutritionist well acquainted with gluten and dairy sensitivities may also be necessary and the commencement of an elimination diet together with nutritional support may be required.
  4. Psychological Assessment – Standardised age-appropriate intelligence tests together with performance tests such as reading, spelling, speed of handwriting, written expression, silent comprehension, maths are considered essential.
  5. Referral for vision testing by a behavioural optometrist may be necessary as many LD/ADHD children have poor accommodation and convergence which can be remediated either with exercises (if the child is compliant) or with syntonics and glasses. An assessment of CADP may also result from this assessment.

  6. Neuro-psychophysiological Assessments

QEEG assessment to assess brain functioning and comorbidities is essential. QEEG results will determine the appropriate protocol for neurofeedback training before remediation of learning difficulties begins.

CAPD assessment to ascertain the extent of the disorder as well as auditory and visual processing speed and ear dominance is vital before sound therapy commences.

Screening for retained primitive reflexes may result in chiropractic or cranio-sacral work before exercises to inhibit these reflexes begins because structural anomalies can impede progress.

Interventions

Education, early detection and intervention are the best strategies as unresolved learning difficulties and ADHD set the stage for future outcomes.

Educational Institutions

This group includes preschool teachers, administrators, District Guidance Officers, District School Counsellors, classroom teachers, specialist itinerant support teachers (emotionally disturbed, vision and hearing impaired, Reading Recovery teachers), and most importantly those who sit on committees to determine funding applications for students with learning disabilities. All need to be thoroughly familiar with the differential diagnosis required in such cases and of the interventions and assessments that are currently available in order to guide their policies and practices.

The educational management of children with learning difficulties is a whole school responsibility and is a collaborative venture between teachers, parents, students, psychologists, speech therapists and medical professionals. It begins with being aware of the need to change in order to support these individuals in their classrooms [180].

Whole School responsibility includes:

Therefore teachers need to:

Students need to be:

(Source: Spencer[179] and Giorcelli[180] ADHD conference 1995 with revisions and inclusions)

Adapting the curriculum and accommodating the needs of students with learning difficulties requires radical rethinking and benefits all students. The committee needs to be aware that the above-recommended whole school strategies were successfully initiated at a private school here in Sydney in 1994. These results were reported at the 1995 conference on ADHD hosted by the LD Coalition of NSW. Despite the fact that the keynote speaker was Loretta Giorcelli, a name familiar in the NSW Department of Education, there were only two school counsellors present at that conference.

Teacher education courses need to:

Health & Caring Professions

This group includes, staff at baby and community health centres, childcare workers in long day care centres, preschool staff, nurses, general practitioners, paediatricians, psychiatrists, and community support groups as learning difficulties are often apparent before the age of two years.

Extensive re-education in this sector is vital if we are to stop using children as "uncontrolled experiments".

Courses in nutrition, herbal medicine and alternative therapies that have proven to be effective and that have caused no harm need to be added to medical school curricula. Naturally, these courses must be conducted by leading and practising practitioners in their fields.

Attitudes in the community are changing and the medical profession needs to learn its lessons from toxicology and their own previous disastrous mistakes - mistakes that are causing parents to wholeheartedly reject the pharmacological model and actively search for safer, more natural therapies in the face of intimidation and ridicule. This search however, often takes years, as information about alternative therapies is rarely forthcoming from conventional medical practitioners and adherents of that model. The damage done during that time is unquantifiable.

Parents, Foster-parents, Grandparents

It is this group that needs the most support. Accurate and up-to-date information and alternatives to the medical model is scarce in the general community. Mothers need to be informed and this can only be achieved through general community awareness.

Parent education, maternal health during pregnancy, neonatal care, diet and nutrition are the cornerstones to optimum brain functioning. Education in these matters needs to be totally restructured at every level.

Effective parenting skills courses specifically designed for parents of these children, and stress management and relaxation strategies are needed.

Financial remuneration in the form of improved and adequate benefits for parents, foster parents and grandparents coping with these children also needs investigation. As it currently stands, grandparents receive no government assistance for these children and many of them are in the over 65 age group. The attitudes of those in charge of setting these payments can only change once they are aware of the enormous difficulties experienced in nurturing these children.

Similarly, health care fund rebates do not adequately cover these therapies – with a maximum of $500-00, this rarely covers the cost of initial assessment, let alone equipment costs or the cost of the therapy itself. Government intervention in this area is necessary.

The importance of preventative health measures cannot be overemphasised to mothers and carers. Furthermore, the legalisation of marijuana cannot be allowed no matter what pressure is put upon the government to do so since it manifests as symptoms of ADHD in users.

Food Industry & Advertising

Government regulations which require food manufacturers to truthfully label of all ingredients in food products is mandatory as is the need for all genetically modified foods to be approved before they are available on supermarket shelves. These regulations must be enforced!

Multinational fast food outlets also need tighter regulation. Food outlets must be made to comply with the Safety Foods Act fully disclosing the ingredients on all processed and take- away food products. For example – a requirement to declare all food additives to be visible to potential consumers (especially those with allergies) so that these consumers can in fact make informed and affordable (in terms of health detriment as well as budgetary) choices.

Those food additives that have already been banned in overseas countries need to be withdrawn immediately. See Appendix D (page 53) for a partial list of these additives.

Processed and junk food (which contains a plethora of chemicals, artificial colourings, preservatives, artificial sweeteners, and MSG) that pervades school and hospital canteens also needs re-evaluation. These foods of which white flour products (gluten, phosphates and the preservative 282-calcium propionate) are the most deadly offenders seconded only by dairy products (casein) and carbonated drinks which contain varying amounts of caffeine and artificial sweeteners such as aspartame, have been shown to exacerbate neurological conditions and physical ailments.

Token sponsorships and youth employment (child labour) by multinational fast food outlets such as McDonald’s should not be seen to out-weight the damage to a nation’s youth and health. Sponsorship of sporting events by alcohol companies needs to be banned.

The exorbitantly high price which is paid for unprocessed health food products is exacerbated by the introduction of the GST and the removal of the GST from these products and nutritional supplements is necessary in order to give lower income earners a chance at improving the quality of their health. Incentive schemes for bona fide producers of health food products is also recommended in order to bring these items within the reach of those in most need of these foods/supplements.

Manufacturers of infant formula must be made to include essential fatty acids in those preparations.

 

Summary

Due to repeated failures, misunderstandings, mislabellings and all other emotional mishaps, individuals with LD's usually develop problems with their self-esteem and self-confidence. They are called lazy, stupid, dumb, "space cadets" and are the subject of many parent-teacher conferences and staff room conversations. For many of the adults seen at this clinic, school was a place where their spirits were broken and who therefore never got a chance to achieve their potential. It is time that the community realised that this is not a minor problem that can be ignored. These are never just individual problems. For each person directly affected by learning disabilities and ADHD there are many more: family, friends, peers, employers and citizens- all of whom suffer emotionally and financially because of these conditions.

The suffering that is endured by learning disabled children in the current school system and at the hands of some members of the medical profession and the attendant psychological scarring is hard to quantify, but it impacts on their motivation, their emotional well-being and often their behavioural stability. There are no magic cures to break this destructive cycle and a better theoretical understanding and awareness of underlying factors will defuse the guilt and blame, and allow children, parents and teachers to concentrate on the more important task of improving the skills of these children and preserving their dignity in the process.

It is the contention of this paper that the current accepted medical and educational practices contribute to these disabilities, and unless a radical shift in paradigm occurs, these conditions will continue to be exacerbated by the pharmacological approach and ineffective cognitive behaviour therapy approaches. The interventions outlined are already in common use in Europe, Asia and America because they provide maximum benefit and no harm and because they seek to correct and resolve the underlying factors that have led to the symptoms in the first place.

The multimodal approaches based on the Learning Pyramid (page 13) and used at this clinic have too many variables to be studied in a randomised controlled trial. Also it would be unethical to preclude some children from best practice and use them as guinea pigs just to provide comparison data. On the other hand, using effective diagnostic tools and pre-treatment measures as comparison data with post treatment outcome measures provides ethical, evidence-based practice.

The brain is "the hardware of your soul" and as such "is the very essence of a human being"[16].

While the best intervention will always be prevention, the early and accurate differential assessment of brain function and other contributing physiological factors, together with the non-pharmacological interventions discussed in this paper, offer learning disabled and attention deficit children the opportunity for amelioration of their difficulties with all the life-enhancing and life-affirming progress this implies.

Conclusion

This group of children who suffer from learning disabilities and ADHD may, through the search for answers to their difficulties, light the path to improved mental and physical health for every industrialised nation in the world. The efficacy of interventions based on the results of neurological, nutritional and other physiological assessments as precursors to educational assessment and intervention has wide-ranging implications for both individuals and society.

To reiterate, this crucial work requires an interdisciplinary panel of qualified and experienced professionals from psychology, medicine, psychiatry, speech pathology, occupational therapy, nutrition and, of course, education. Additionally, parents and members of support groups and the wider community including business leaders would no doubt, enhance the investigation. Such an investigation would be the first step in changing community attitudes and increasing public awareness.

The cornerstone of change is education and attitudinal change. Learning disabled and attentional deficit children are precious resources for our society, with each one having intrinsic value in their own right. It is up to all of us concerned, professionals and lay people alike to open our minds, keep ourselves informed and advocate for best practice for these children.

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APPENDIX A

DSM-IV CRITERIA FOR ADD/ADHD[1]

A. Either (1) or (2)

(1) six (or more) of the following symptoms of inattention have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

Inattention

(a) often fails to give close attention to details or makes careless mistakes in schoolwork, work or other activities

(b) often has difficulty sustaining attention in tasks or play activities

(c) often does not seem to listen when spoken to directly

(d) often does not follow through on instructions and fails to finish schoolwork, chores or duties in the workplace (not due to oppositional behaviour or failure to understand instructions)

(e) often has difficulty organising tasks and activities

(f) often avoids, dislikes or is less reluctant to engage in tasks that require sustained mental effort (schoolwork, homework)

(g) often loses things necessary for a task or activities (e.g. toys, school assignments, pencils, books or tools)

(h) is often easily distracted by extraneous stimuli

(i) is often forgetful in daily activities

(2) six (or more) of the following symptoms of hyperactivity/impulsivity have persisted for at least six months to a degree that it is maladaptive and inconsistent with developmental level:

Hyperactivity

(a) often fidgets with hands or feet or squirms in seat

(b) often leaves seat in classroom or in other situations in which remaining seated is expected

(c) often runs about or climbs excessively in situations in which it is inappropriate (in adolescents or adults, may be limited to subjective feelings of restlessness)

(d) often has difficulty playing or engaging in leisure activities quietly

(e) is often "on the go" or acts as if "driven by a motor" often talks excessively

Impulsivity

(a) often blurts out answers before questions have been completed

(b) often has difficulty awaiting turn

(c) often interrupts or intrudes on others (e.g. butts into conversations or games)

B. Some hyperactive-impulsive or inattentive symptoms that caused impairment were present before the age of 7 years.

C. Some impairment from the symptoms is present in two or more settings (e.g. at school [or work] and at home).

D. There must be clear evidence of clinically significant impairment in social, academic or occupational functioning.

E. The symptoms do not occur exclusively during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder and are not better accounted for by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder).

Coding based on type:

314.01 Attention-Deficit/Hyperactivity Disorder, Combined Type: if both Criteria A1 and A2 are met for the past 6 months

314.00 Attention-Deficit/Hyperactivity Disorder, Predominantly Inattentive Type: if Criterion At is met but Criterion A2 is not met for the past 6 months

314.01 Attention-Deficit/hyperactivity Disorder, Predominantly Hyperactive Type: if Criterion A2 is met but Criterion At is not met for the past 6 months

314.9 Attention-Deficit/Hyperactivity Disorder Not otherwise Specified: prominent symptoms of inattention or hyperactivity/impulsivity that do not meet the criteria for Attention Deficit Hyperactivity Disorder

Coding note: For individuals (especially adolescents and adults) who currently have symptoms that no longer meet full criteria, "In Partial Remission" should be specified.

APPENDIX B - SOME ADVERSE EFFECTS OF STIMULANTS

[Source: Talking Back to Ritalin, Dr Peter Breggin, 1998 (pg 12) *Depression & sadness added by Breggin Modified from the DEA (1995b)]

Organ system affected

Ritalin (Methylphenidate)

Dexamphetamine (Amphetamines)

Cardiovascular

Palpitations

Tachycardia (abnormally increased heart rate)

Increased blood pressure

Palpitations

Tachycardia

Increased blood pressure

Central Nervous System

Excessive CNS stimulation (can cause convulsions)

Psychosis (toxic or organic)

* Depression or sadness

Dizziness (Vertigo)

Headache

Insomnia

Nervousness

Irritability

Attacks of Tourette’s or other tic syndromes

Excessive CNS stimulation

Psychosis

* Depression/sadness

Dizziness

Headache

Insomnia

Nervousness

Irritability

Attacks of Tourette’s or other tic syndromes

Gastrointestinal

Anorexia (loss of appetite)

Nausea

Vomiting

Stomach pain

Dry mouth

Anorexia

Nausea

Vomiting

Stomach pain

Dry mouth

Endocrine/metabolic

Weight loss

Growth suppression

Weight loss

Growth suppression

Other

Blurred vision

Leucopoenia (low white blood cell count)

Hypersensitivity reaction

Anaemia

Blurred vision

Skin rash or hives

FUNCTIONS OF THE BRAIN IMPAIRED BY STIMULANTS

(Source: P Breggin,MD, "Talking Back to Ritalin", (1998) page 44)

Area

Where Located

Effects of Dysfunction

Cerebral Cortex

Outer surface of the brain

Impairs higher mental activities, including intelligence and sensory perception

Frontal Lobes

Front of the brain

Impairs initiative and autonomy, reason, empathy and social awareness, insight and judgement- the most human functions. Can cause emotional blunting and zombie-like behaviour.

Limbic System

Widespread, beneath the frontal lobes

Affects regulation of emotions, and usually produces indifference and apathy or euphoria. Can cause zombie-like behaviour.

Basal Ganglia

Middle of the brain

Causes abnormal movements and can cause emotional blunting and zombie-like behaviour.

Temporal lobes including Hippocampus

Lower sides and undersurface of the brain

Impairs memory and learning

Parietal lobe

Towards the back surface of the brain

Impairs integration and understanding of sensory perception, language and sense of smell.

Cerebellum

Lower posterior of brain

Affects regulation of muscle tone, posture, gait and skilled coordination.

Hypothalamus

Small area of undersurface of brain above pituitary gland

Impairs temperature control, appetite and hormonal function, including pituitary gland

Pituitary Gland

Base of the brain

Can impair growth, thyroid, adrenal and sexual functions and the overall reaction to stress.

Reticular Activating System (RAS)

Core of the brain

Dysfunction within the RAS blunts energy, alertness, self-awareness and responsiveness.

Spinal Cord

Begins at the base of the brain and extends downwards through the vertebral column

Affects nerves that spread throughout the body, especially impaired are reflexes and muscle tone.

MEDICAL DISORDERS THAT CAN CAUSE ADHD-LIKE SYMPTOMS

There are many medical disorders that can mimic ADHD/ADD. Thus it is important to eliminate the following disorders before a diagnosis is made. These include:

Prenatal factors – poor maternal care, eclampsia (hypertensive disorder during pregnancy), maternal use of cigarettes, alcohol and prescription, recreational and illegal drugs

Birth and perinatal complications – birth injury, hypoxia (blue baby), toxaemia, prolonged labour, low birth weight, postmaturity/prematurity

Inborn errors of metabolism – phenylketonuria (PKU)

Stresses in infancy – malnutrition, abandonment

Trauma and anoxia (absence of oxygen) – any head injury, including mild closed head injury; shaking (when parents shake babies in anger); anoxia from any cause, such as drowning, smothering, choking and strangulation

Toxic exposures – lead, mercury, carbon monoxide poisoning, air pollutants

Infection – meningitis, encephalitis, almost any fibrile illness (elevated temperature)

Neurological disorders – seizures (especially absence seizures), Sydenham’s chorea, mental retardation from any cause, drug-induced akathisia (inner tension and hyperactivity)

Other specific diseases and disorders – Insulin-dependent diabetes, cerebral vascular accident, brain tumour, chemotherapy for cancer, chronic renal disease, Lupus with CNS inflammation, iron-deficiency (anaemia), hormonal disorders (most commonly thyroid), vitamin deficiencies

Physical disabilities – visual impairment from any cause, hearing impairment from any cause including ear infections

Fatigue and insomnia –any cause of chronic tiredness or lack of sleep, Chronic Fatigue Syndrome

Hunger – many children from affluent families do not eat properly and may be hungry in school. Sometimes these children suffer from eating disorders.

Pain – any source of pain, including hidden infections (ears), stomach and intestinal cramps (constipation), headache.

 

MEDICATIONS THAT CAN CAUSE ADD-LIKE SYMPTOMS

Most psychiatric and neurological medications including:

Stimulants (Ritalin, Dextroamphetamine, Adderall, Cylert, Caffeine)

Antidepressants (including SSRI’s such as Prozac, Paxil, Luvox, Zoloft)

Neuroleptics or antipsychotics (Melleril, Haldol, Largactil, Navane, Risperidone etc.)

Minor tranquillisers, sedatives or sleeping medications (Valium, Normison, Librium, Xanax, Ativan etc.)

Antiepileptic medication (Dilantin, Tegeratol, Epalim, Depakote, Zarontin)

Barbiturates (phenobarbitol, amobarbitol, or Amytal, Butisol, Nembutal, Seconal)

Mood stabilisers (Lithium, Catapress, Depakote, Tofranil, Verapamil)

Asthma medications

Ephedrine and pseudophedrine, Theophylline, Antihistamines

Over-the-counter cold, allergy and sinus medications

Most contain antihistamines or mild stimulants that can cause ADD-like symptoms.

Over-the-counter sleeping medications

Any drug that can make you sleepy can impair alertness and impair concentration.

Steroids

Prednisone, Anabolic steroids (used to build muscle mass)

Some antibiotics

Antibiotics frequently cause fatigue. A number have been associated with mental abnormalities, including various penicillins and cephalosporins (Ceclor).

All drugs that are abused

Amphetamine, methamphetamine, Ritalin, cocaine, ecstasy, Phencyclidine (PCP), d-Lysergic acid (LSD), Marijuana, Alcohol, All sedatives, hypnotics, minor tranquillisers including halcicon, Valium, Ativan, Xanax, Dalmane, Klonopin

APPENDIX C

EEG BIOFEEDBACK IN THE TREATMENT OF ADHD

Alhambra, M.A., Fowler, T.P., and Alhambra, A. A. (1995). EEG Biofeedback: A New Treatment Option for ADD/ADHD. Journal of Neurotherapy, 1(1), 39-43.

Arnold, L.E. (1995). Some nontraditional (unconventional and/or innovative) psychosocial treatment for children and adolescents: Critique and proposed screening principles. Special Issue: Psychosocial treatment research. Journal of Abnormal Child Psychology, 23, 125-140.

Janzen, T., Graap, K., Stephanson, S., Marshal(, W. et al. (1995). Differences in baseline EEG measures for ADD and normally achieving preadolescent males. Biofeedback & Self Regulation, 20(l), 65-82.

Kaiser, D. A., & Othmer, S. (1998). Efficacy of SMR-beta neurofeedback on aftentional processes. Unpublished paper available at http://www.eegspectrum.com

Linden, M., Gevirtz, R., Isenhart, R, & Fisher, T. (1996). Event-related potential of subgroups of children with attention deficit hyperactivity disorder and the implications for EEG biofeedback. Journal of Neurotherapy, 1, 40-49.

Linden, M., Habib, T., & Radojevic V. (1996). A controlled study of the effects of EEG biofeedback on cognition and behavior of children with attention deficit disorder and learning disabilities. Biofeedback & Self Regulation, 1, 35-49

Lubar, J.F. (11989). Electroencephalographic biofeedback and neurological applications. IN: J. V. Basmajian, (Ed.), Biofeedback: Principles and practice for clinicians (3rd ed.). Baltimore: Williams & Wilkins, pp. 67-90.

Lubar, J.F. (1991). Discourse on the development of EEG diagnostics and biofeedback for attention-deficit/hyperactivity disorders. Biofeedback & Self Regulation, 16 (3), 201-225.

Lubar, J. F. (11995). Neurofeedback for the management of aftention-deficit/hyperactivity disorders. In: M. S. Schwartz (Ed.). Biofeedback: A Practitioner's Guide. New York: Guilford, pp. 493-522.

Lubar, J.F. & Shouse, M.N. (1976). EEG and behavioral changes in a hyperkinetic child concurrent with training of the sensorimotor rhythm (SMR): a preliminary report. Biofeedback & Self Regulation, 1(3), 293-306.

Lubar, J. F., Swartwood, M. 0., Swartwood, J. N., & O'Donnell, P. H. (1995). Evaluation of the effectiveness of EEG neurofeedback training for ADHD in a clinical setting as measured by changes in TOVA scores, behavioral ratings, and WISC-R performance. Biofeedback and Self- Reg ulation, 29(l), 83-99.

Lubar, J.0. & Lubar, J.F. (1984). Electroencephalographic biofeedback of SIVIR and beta for treatment of attention deficit disorders in a clinical setting. Biofeedback & Self Regulation, 9(l), 1-23.

Pfurtscheller, G. (1992): Event-related synchronisation (ERS): an electrophysiological correlate of control areas at rest. Electroencephalography and Clinical Neurophysiology. 83, 62-69.

Plude, David B. (1996). New technology: A biological understanding of attention deficit hyperactivity disorder and its treatment. Journal of Neurotherapy, 1, 10-14.

Rasey, H. W., Lubar, J. F., McIntyre, A., Zoffuto, A.C., & Abbott, P. L. (1996). Journal of Neurotherapy, 2, 15-21. EEG biofeedback for the enhancement of attentional processing in normal college students. Journal of Neurotherapy, 1, 15-21.

Rossiter, T. R., & La Vaque, T. J. (1995). A comparison of EEG biofeedback and psychostimulants, in treating attention deficit/hyperactivity disorders. Journal of Neurotherapy, 1, 48-59.

Shouse, M.N. & Lubar, J.F. (1978). Physiological basis of hyperkinesis treated with methylphenidate. Pediatrics 62(3), 343-351.

Shouse, M.N. & Lubar, J.F. (1979). Operant conditioning of EEG rhythms and Ritalin in the treatment of hyperkinesis. Biofeedback & Self Regulation, 4(4), 299-312.

Sterman, M.B. (1996). Physiological origins and functional correlates of EEG rhythmic activities: implications for self-regulation. Biofeedback & Self Regulation, 21 (1), 3-33.

Sterman M.B. & Kaiser D (2000): Comodulation: A new QEEG Analysis Metric for Assessment of Structural and Functional Disorders of the CNS. In press.

Tan, G. (1997). Attention-deficit hyperactivity disorder: pharmacotherapy and beyond. Postgraduate Medicine 101(5), 201-204.

Tansey, M. A. (1990). Righting the rhythms of reason: EEG biofeedback training as a therapeutic modality in a clinical office setting. Medical Psychotherapy, 3, 57-68.

Tansey, M.A. (1986). A simple and a complex tic (Gilles de la Tourette's syndrome): Their response to EEG sensorimotor rhythm biofeedback training. International Journal of Psychophysiology, (2), 91-97.

Wolraich, M.L. & Baumgaertel, A. (1997). The practical aspects of diagnosing and managing children with attention deficit hyperactivity disorder. Clinical Pediatrics, 36, 497-504.

EEG BIOFEEDBACK IN THE TREATMENT OF LEARNING DISABILITIES

Cunningham, M.D. & Murphy, P.J. (1981). Clinical effects of bilateral EEG biofeedback on verbal, visual-spatial & creative skills in learning disabled male adolescents. Journal of Learning Disabilities. 1(4), 204-208.

Linden, M., Habib. T., & Radojevic, V. (1996). A controlled study of theeffects of EEG biofeedback on cognition and behaviour of children with attention deficit disorder and learning disabilities. Biofeedback & Self-Regulation, 21, 35-49

Lubar, B., Calhoun, P. et al. (1985). Learning Disabilities, 18(7), 403ff.

Lubar, J.F. (1985). EEG biofeedback and learning disabilities. Theory into Practice. Journal of Learning Disabilities 24(2), 106-111.

Tansey, M.A. (1984). EEG sensorimotor rhythm biofeedback training: Some effects on the neurologic precursors of learning disabilities. International Journal of Psychophysiology, 1(2), 163-177.

Tansey. M.A. (11985). Brainwave signatures--an index reflective of the brain's functional neuroanatomy: Further findings on the effect of EEG sensorimotor rhythm biofeedback training on the neurologic precursors of learning disabilities. International Journal of Psychophysiology, 3(2), 85 -99.

Tansey, Michael A. (1990). Righting the rhythms of reason: EEG biofeedback training as a therapeutic modality in a clinical office setting. Medical Psychotherapy: An International Journal, 3, 57-68.

Tansey, M.A. (1991). Wechsler (WISC--R) changes following treatment of learning disabilities via EEG biofeedback training in a private practice setting. Australian Journal of Psychology, 43(3), 147-153.

Tansey, M.A. (1993). Ten-year stability of EEG biofeedback results for a hyperactive boy who failed fourth grade perceptually impaired class. Biofeedback & Self Regulation, 18 (1), 33-44.

Tansey, M.A., & Bruner, R.L. (1983). EMG and EEG biofeedback training in the treatment of a 1 0-year-old hyperactive boy with a developmental reading disorder. Biofeedback & Self Regulation, 8(l), 25-37.

Tansey M.A., Tansey. J.A.. & Tachiki, K.H. (1994). Electroencephalographic cartography of conscious states. International Journal of Neurosciences, 77, 89-98.


EEG BIOFEEDBACK IN THE TREATMENT OF EPILEPSY

Andrews, D.J. and Schonfeld, W.H. (1992). Predictive factors for controlling seizures using a behavioural approach. Seizure, 1, 111-116.

Ellenson. B. and Klove. H. (1976). Clinical application of biofeedback training in epilepsy. Scandinavian Journal of Behavior Therapy, 133-144.

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Finley, W.W., Smith, H.A. and Etherton, M.D. (1975). Reduction of seizures and normalization of the EEG in a severe epileptic following sensorimotor biofeedback training: Preliminary study. Biological Psychiatry, 2, 189-203.

Kaplan, B.J. (1975). Biofeedback in epileptics: Equivocal relationship of reinforced EEG frequency in seizure reduction. Epilepsia, 16, 477-485.

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APPENDIX D

Table 10.1, pp 290 Dr. Charles Krebs - A Revolutionary New Way of Thinking[181]

Food Additives and Preservatives known or suspected of being associated with adverse behavioural or psychological reactions

Colours

Known/Suspected of being associated with adverse reactions

102 Tartrazine

Hyperactivity, migraine, asthma, rhinitis, blurred vision, insomnia, skin reaction

107 Yellow 2G

Asthma, hyperactivity, skin reactions

110 Sunset Yellow FCF

Asthma, hyperactivity, skin reactions, swelling, gastric upset, vomiting, possibly carcinogenic

120 Cochineal

Hyperactivity

122 Azorubine

Asthma, hyperactivity, skin reactions, swelling, water retention

123 Amaranth

Asthma, hyperactivity, skin reactions, possibly carcinogenic

124 Brilliant Scarlet 4R

Asthma, hyperactivity, skin reactions

127 Erythrosine

Light sensitivity, hyperactivity, overactive thyroid, brain dysfunction, possibly carcinogenic

132 Indigo carmine

Nausea, vomiting, high blood pressure, skin reactions, breathing difficulty, hyperactivity

133 Brilliant Blue FCF

Hyperactivity

142 Green S

Asthma, hyperactivity

150 Caramel

Hyperactivity, diarrhoea

151 Brilliant Black BN

Hyperactivity

155 Brown HT

Asthma, hyperactivity, skin reactions

 

Flavour Enhancers

 

620 L-Glutamic acid

Muscle tightening, numbing effects, thirst, nausea, palpitations, dizziness, fainting, headaches, cold sweat, asthma, hyperactivity

621 Monosodium glutamate

Muscle tightening, numbing effects, thirst, nausea, palpitations, dizziness, fainting, headaches, cold sweat, asthma, hyperactivity

622 Monopotassium glutamate

Nausea, vomiting, diarrhoea, abdominal cramps, headache, asthma, hyperactivity

623 Calcium di-L-glutamate

Asthma, hyperactivity

627 Disodium guanylate

Asthma, hyperactivity, gout

 

 

Preservatives

 

210 Benzoic acid

Hyperactivity, asthma, skin reactions, gastric irritations, brain dysfunction

211 Sodium Benzoate

Hyperactivity, asthma, skin reactions

212 Potassium Benzoate

Hyperactivity, asthma, skin reactions

213 Calcium Benzoate

Hyperactivity, asthma, skin reactions

216 Propylparaben

Hyperactivity, asthma, contact dermatitis, numbing affect on the mouth

218 Methylparaben

Hyperactivity, asthma, skin reactions

220 Sulphur Dioxide

Hyperactivity, asthma, gastric irritations

221 Sodium Sulphite

Hyperactivity, asthma, gastric irritations, skin reactions

222 Sodium bisulphite

Hyperactivity, asthma, gastric irritations, skin reactions

223 Sodium metabisulphite

Hyperactivity, asthma, gastric irritations, skin reactions

224 Potassium metabisulphite

Hyperactivity, asthma, gastric irritations, skin reactions, collapse

250 Sodium nitrite

Hyperactivity, breathing difficulties, pallor, nausea, vomiting, dizziness, headaches, low blood pressure, collapse

251 Sodium nitrate

Hyperactivity, possibly carcinogenic

 

 

Ani-oxidants

 

320 Butylated hydroxyanisole

Hyperactivity, skin reactions, asthma, possibly carcinogenic

321 Butylated hydroxytoluene

Hyperactivity, skin reactions, asthma, possibly carcinogenic

 

APPENDIX E

THE RELATIONSHIP BETWEEN SUBSTANCE ABUSE (PRIMARILY MARIJUANA) AND ADHD

(Source: Anderson 1997, summarised by Susan Johnston and revised by Rosemary Boon)

Contrary to popular belief, marijuana is not harmless and is in fact addictive. According to a study conducted by Dr. Kadden (1997) from the University of Conneticut Health Centre, marijuana addiction is both psychological and physiological.

Many participants in the three year study expressed feelings that they could not cope or even function adequately without marijuana, and that their addiction interfered with leading a normal life. Further, they felt that they needed treatment for their addiction.

The following is a summary by Susan Johnston of findings from similar research by neuropsychologist, John Anderson (Sydney 1997) which was presented at the "ADDult NSW" Awareness Afternoon on Sept 6th 1997.

1.40% of children with ADHD are predisposed to developing substance abuse during adolescence/adulthood.
Of the ADHD population that are poly-substance users, 61% smoke marijuana.

30-40% of substance abusers (marijuana, heroin, methadone) have ADD. There are 18,000 people on methadone in Sydney alone.

2. Many of the behavioural changes in marijuana users are the same as those of ADHD, hence it is often difficult for clinicians to differentiate between ADHD and marijuana use. These specific behaviourial changes in cannabis users include: significant decrease in academic ability, increased depression, increased anxiety, increased impulsivity, significant increase in respiratory infections (colds, sniffles), short term memory problems increase, a-motivational syndrome (lack of interest/enthusiasm in things previously enjoyed), temporal distortions, reaction time slows, reaction time slows, and changes in appetite.

3. Although THC is the active ingredient that causes the high, there are 61 other agents in marijuana. Since it is not a pure substance, individual reactions vary.

4. Two of the cannaboids (CBD & CNN) found in marijuana have been demonstrated by research to affect chromosomal structure. In males, it results in spermatogenesis and in women, actively affects the shape of the ovum. The gene that is affected is the same gene implicated in ADHD - on the short arm of chromosome 6.

5. Marijuana is fat soluble, and the brain and gonads are the major fatty tissues in the body. Marijuana alters testosterone levels and males who have ADD tend to have mood swings exacerbated by continued use.

6. Smoking one joint a day, three times a week, for six months, results in changes in brain physiology that can be detected three to five years later.

7.Since marijuana decreases the amount of T-cells in the blood, the immune system is weakened.

8. Marijuana contains 50-70% more carcinogens than tobacco and there is a higher incidence of jaw, throat and tongue cancer among marijuana users.

9. The cardio-vascular system is also adversely affected since marijuana deprives the brain of oxygen. When the blood flow to the brain is decreased by 4% significant problems in terms of brain function result. In dementia patients blood flow is decreased by 4%, ADHD 8-12%, schizophrenia 12-15%, marijuana users 10-15%.

10. Long term users may develop drug induced psychosis (similar to schizophrenia with paranoia and delusions). One in ten of those with drug psychosis will commit suicide unless treated in the first two years (usually poly users). Other than those who develop drug induced psychosis and cancer, research demonstrates that all other effects are fully reversible with total abstinence.

In young children and adolescents, 80% of the ADHD population have a dopamine/noradrenaline difficulty, and 20% a dopamine problem only. The brain changes with age and noradrenaline usually normalises. Thus the adult ADHD brain is primarily characterised by a dopamine and sometimes a serotonin dysfunction. The inattentive type of ADD is also characterised by predominantly dopamine and serotonin dysfunction. If an ADD adult smokes marijuana, the doparnine receptors are filled with THC instead of dopamine. This exacerbates the problem as it causes an imbalance in other neurotransmitters.

There is little point in using medication or neurofeedback training for ADHD if marijuana smoking continues as the medication becomes ineffective unless massive doses are taken. Furthermore, an inordinate number of neurofeedback training sessions will be required. Increasingly stronger drugs are required and the progression from marijuana to speed (amphetamines) to heroin is likely. If those with ADHD are treated more appropriately, then maybe they can eventually get off methadone, thus actively treating the disorder, and not just the symptoms.