A.D.H.S. Anhang 8
[John-John Brian Lottering theories for ADHS]
The relative efficacy of Advanced Brain Food® and a Homeopathic Complex (Quietude® in the management of Attention Deficit Hyperactivity Disorder (ADHD) in
males between the ages of 8 and 13 years.
ADD/ADHD is one of the most commonly diagnosed disorders of childhood development (Kendall and Hammen, 1995; Venter, 1996).
It is believed to affect between 3 - 5% of all children of school age and although it also affects adults and adolescents, the figures here are not available (DSM-IV, 1994).
The values for females are often under reported due to the fact that they go undiagnosed as their symptoms are attributed to emotional problems common in young girls (Kendall and Hammen, 1995/Berkow et al. 1992) and they are less aggressive and active than boys, which makes them less noticeable (Picton, 1997).
The diverse and conflicting opinions about ADHD have resulted in confusion for families, care providers, educators and policy makers (NIH Consensus Statement, 1998).
The controversy raises questions concerning the literal existence of this disorder, whether it can be reliably diagnosed and, if treated, what interventions are most effective (NIH Consensus Statement, 1998/American Psychiatric Association, 1994).
ADD/ADHD characterised predominantly by developmental inappropriate inattention +/o. impulsivity and/or hyperactivity (Woods and Ploof, 1997).
Children with ADD/ADHD usually have functional impairment across multiple settings including their home, school and peer relationships (NIH Consensus Statement, 1998/Breggin, 2003).
The symptoms characteristic of this disorder namely hyperactivity, short attention span and impulsiveness are thought to suggest central nervous system involvement (Castellanos et al. 1996/DSM-V, 1994).
Diagnosis is a problem as it has been shown that many children are not identified or otherwise falsely identified by their paediatrician or doctor for a number of reasons (Breggin, 2003/Richardson, Hamley and Sassone, 2000). Testing of children is often limited and not comprehensive enough, case histories may not be detailed enough and often the influence of a teacher or school is enough to encourage a doctor to prescribe stimulant medication (NIH Consensus Statement, 1998; Picton, 1997/Oltmanns
and Emerly, 1995). The most commonly used diagnostic method is from the Diagnostic and Statistical Manual-IV (1994).
Attention Deficit Hyperactivity Disorder is a heterogeneous behavioural disorder with multiple possible aetiologies. These may be classified into the following causations: environmental factors, central nervous system (CNS) insult, genetic origins and, neurochemical/neuroanatomical factors (Goldman, 1998).
The brain consists of modules specialised for processing specific data. These modules are autonomous to a degree in both function and neural representation (Frei et al. 2001).
The outermost layer of the brain represents the cerebral cortex. The cortical (frontal) section of the brain is related to learning and thinking.
The layer underneath, the sub-cortex, comprises a relay system that is involved in sending messages to the processing and memory parts of the brain (Rapoport, 1995)
This sub-cortical system consists of the brain stem‘s reticular activating system, thalamus, hypothalamus and basal ganglia (Guyton, 1989/Rapoport, 1995).
Laufer et al. (1957), who proposed that the symptoms of ADHD were caused by ―diencephalic dysfunction, reported the first anatomical-based hypothesis for the cause of hyper-kinesis.
Recent research suggests that ADHD children generally have impaired functioning in the cortical and subcortical areas (Hynd et al. 1993). In particular, frontal lobe and prefrontal lobe dysfunction have been suggested (Hynd et al. 1991).
Anatomic neuro-imaging studies are converging in revealing differences in children with ADHD, compared to age-matched controls (Castellanos, 2000; Greenhill et al. 2002).
ADHD children notably have a smaller brain volume (4% decrease from normal), as well as a smaller caudate nucleus, globus pallidus, anterior frontal cortex and sub-region of the cerebellar vermis (Castellanos, 2000). These volumetric differences appear early and are not secondary to stimulant medication.
In the early 1990s, many functional imaging techniques were used in a variety of clinical settings to image the brains of ADHD patients in comparison to normal control subjects.
Swanson et al. (1998) integrated the findings across multiple studies and calculated the standardised effective size.
It was found that there is a consistent moderate reduction of about 10% of the size in healthy controls in the frontal lobes (dorsolateral prefrontal cortex and anterior cingulate), basal ganglia (caudate nucleus and globus pallidus), and some regions of the corpus callosum (rostrum and splenium), which link frontal and parietal brain regions (Swanson et al. 1998/Castellanos, 2000).
A recent study done by the National Institute of Mental Health found that three structures in the right brain-prefrontal cortex, caudate nucleus and globus pallidus were affected by ADHD (Castellanos, 2000).
These areas were smaller than those of children without ADHD, thus ADHD is thought to be rooted in an inability to inhibit thoughts.
Furthermore, ADHD children exhibit smaller frontal lobes and less activity in the striatum, which is a major dopamine-rich supply for the frontal lobes (Castellanos, 2000).
The majority of ADHD children exhibit decreased perfusion in the pre-frontal cortex with intellectual stress (Amen et al. 1997).
Brain scans have identified a clear-cut chemical abnormality in people with attention deficit-hyperactivity disorder, a problem that makes life difficult for an estimated 3 to 5% of US school children
scientists say (New York Times Syndicate - December 16, 1999).
With the development of imaging and isotope scanning techniques, studies of anatomy and glucose metabolism of ADHD children have been made possible (Swanson et al. 1998).
Positron emission tomography (PET) scan studies have shown reduced brain glucose utilisation, particularly as related to the right frontal lobe, in ADHD children (Zametkin and Rapoport, 1987).
Furthermore, ADHD children show decreased blood flow in the frontal lobes (Hynd et al. 1993).
In a recent study, it was shown that the rate at which the brain uses glucose, its main energy source, is lower in subjects with ADHD than in subjects without ADHD (Zametkin et al. 1990).
Analysis of electroencephalograms (EEGS) of boys with ADHD has found increased slow-wave activity in the frontal regions (Hynd et al. 1991).
Although this research suggests frontal lobe dysfunction, some researchers believe the neurological basis for ADHD should not be limited to frontal immaturity or abnormality (Baizier, 2001). They believe ADHD is related to more widespread dysfunction in the brain (Benson, 1991).
These results suggest that ADHD may have an organic basis and that dysfunction can be localised to cortical and striatal regions in the brain (Woods and Ploof, 1997; Castellanos 2000).
Neurochemical hypotheses are based on the effects of neurotransmitters (Zametkin et al. 1990).
These are chemicals that relay messages from one neuron to another through synapses (Castellanos, 2000).
The neurotransmitters that function within the attentional system are the catecholamines, which function in the neural circuits that control motivation and motor behaviours, including activity level, restlessness, and responsivity (Ballard et al. 1997).
The neurochemical theories postulate that behaviours seen in ADHD are due to a dysfunction in the neurotransmitter system.
Supporting this theory is the beneficial effect that certain medications, which have a direct effect on the neurotransmitters in the body, have on the disorder (Bazier, 2001).
ADHD is a neurobiological disorder with anatomic and functional impairments in the brain, leading to monoamine dysregulation and frontostriatal alterations in neural circuitry (Herscu, 1995).
There is strong evidence that the catecholamines, dopamine and norepinephrine are important in the pathophysiology of ADHD (Castellanos, 2000).
Dysfunction of dopaminergic and noradrenergic systems are constantly implicated in ADHD (Baizier, 2001; Holford, 2001).
Dopamine and norepinephrine are important neuromechanisms governing focused attention (Castellanos, 2002).
Dopamine is a neurotransmitter in the catecholamine family that functions in the brain. Hypothesis is based on an animal model of hyperactivity, biochemical and on clinical pharmacological studies with ADHD subjects (Castellanos, 2000/Smalley et al. 2000/Zametkin and Rapoport, 1987).
Some evidence suggests there is a reduction in cerebral turnover of dopamine and decreased dopamine activity (dopaminergic dysfunction) within the brain of an ADD and hyperactive subject (Smalley et al. 2000).
The models of dopaminergic dysfunction cannot account for the findings that dopamine agonists have not proven efficacious when compared to stimulant treatments, nor have dopamine-blocking agents been deleterious (Zametkin and Rapoport, 1987).
More recent studies reveal that hyperactivity and possible poor motor impulse control, in ADHD may result from excess dopaminergic activity in the striatum +/o. nucleus accumbens (Castellanos et al. 1996).
According to Harvard Medical School, current research strongly suggests that ADHD is caused in part by a deficiency of norepinephrine in the ascending reticular activating system, and is thought that stimulant medications, such as Ritalin®, increase the levels of norepinephrine in that part of the brain, as well as probably increasing dopamine levels in the frontal lobes (Breggin, 2000; Rapoport, 1995).
Recent reports suggest that DNA variants of the dopamine D4 receptor gene are associated with the personality trait of Attention Deficit Hyperactivity Disorder (Paterson, 1999).
Boys with a low dopamine D4 receptor gene concentration exhibit significantly more symptoms of ADD/ADHD than boys with normal dopamine D4 receptor genes (Castellanos, 2000).
Many dopamine agonists that stimulate postsynaptic dopamine receptors have been given to patients and were ineffective.
The models of dopaminergic dysfunction cannot account for the findings that dopamine agonists have not proved efficacious when compared to stimulant treatments, nor have dopamine blocking agents been deleterious, unless other hypotheses are put forth (Zametkin and Rapoport, 1987).
Although serotonin has been studied less thoroughly in the neurobiology of ADHD, its role in the pathophysiology of this disorder has recently become an area of intense investigation. Considerable evidence suggests a role for this neurotransmitter in the aetiology of behavioural disorders characterised by disinhibition including alcohol abuse, suicide, bulimia, antisocial personality disorder, conduct disorder and aggression (Castellanos, 2000).
As ADHD is a behavioural disorder largely characterised by deficits in inhibition and is a well-known precursor for many adult disorders of impulse control, a role for 5-Hydroxytryptothan (5-HT) in ADHD has been hypothesised.
Indeed, there is mounting evidence from both human and animal studies that serotonergic neurotransmission is necessary for mediating several of the behaviours present in ADHD (Schoenthaler et al. 1999).
A recent study of a mouse model of ADHD provided evidence which linked serotonin to the control of hyperactive behaviour (Gainetdinov et al. 1999).
All of the studies done have used L-tryptophan, the amino acid precursor to serotonin, and Fenfluramine®, an appetite suppressant that acutely increases and then depletes brain serotonin (Zametkin and Rapoport, 1987).
No significant behavioural changes were seen in any of the ADHD patients tested, decreasing the likelihood of the veracity truth of this hypothesis.
In conclusion, there is accumulating neurobiological evidence pointing towards the role of the serotonin system in ADHD.
The strongest support from existing data suggests that serotonin is responsible, at least in part, for mediating the hyperactive and impulsive components of ADHD behaviour
(Hanna, Ornitz and Hariharan, 1996; Leary, 1994).
Norepinephrine is another neurotransmitter in the catecholamine family.
Kornetsky first proposed this hypothesis in 1970, stating that amphetamine may act as an inhibitor of either norepinephrine synthesis or turnover, or it may block the release
of norepinephrine in the over aroused organism.
This was hypothesised in response to the observations that amphetamine, a sympathomimetic amine, causes a release of norepinephrine and most likely and increase in the rate of turnover. Therefore, ADHD could result from an increase in norepinephrine and amphetamine that may competitively bind to postsynaptic norepinephrine receptors, reducing noradrenergic neuro-transmission (McGough and McCracken, 2000).
Since then, studies have shown that some drugs, proven effective for ADHD, actually alter noradrenergic turnover and may argue for a pathological hyper-functioning of the noradrenergic system in ADHD subjects. Animal studies have shown the opposite effects.
These studies lead to the hypothesis that animal hyperactivity is caused by norepinephrine depletion (Zametkin and Rapoport, 1987).
Each of the specific neurotransmitter hypotheses above have led to either inconclusive or disproving results (World Health Organization, 1999).
Therefore, since the stimulants used to treat ADHD affect multiple transmitters, it was thought that perhaps a dysfunction in the catecholamine neurotransmitters as a group was to blame (Amen et al. 1997/Castellanos et al. 1996).
A series of studies were performed using a group of drugs that also affect multiple neurotransmitters.
They all had immediate and positive behavioural effects on children with ADHD (Castellanos, 2000).
However, the close relationship between the transmitter systems affected and the fact that so many were affected does not illustrate that one was more important that any of the others. Clearly, though, the array of effective agents has served to put to rest any single neurotransmitter hypothesis (Castellanos, 2000/Zametkin and Rapoport, 1987).
The Hypoarousal Theory
Alertness and directed attention depends on the normal functioning of the reticular activating system (RAS) in the brainstem. Incoming sensory stimuli are filtered and sorted before neural impulses are - despatched to the cerebral cortex. Stimuli not relevant to immediate functioning are at this point blocked from conscious awareness (Holford, 2001).
It has been postulated that children with ADHD are continuously in a state of hypo-arousal and are therefore unable to filter out irrelevant and distracting sensory input from their external surroundings (Hanna, Ornitz and Hariharan, 1996). Research has shown that ADHD children have significantly less alpha activity on electroencephalogram (EEG) readings as compared to normal peers (Castellanos et al. 1996/Zametkin et al. 1990).
Goodman and Poillion (1991) have indicated that the majority of causes of ADHD are attributable to organic problems. Their research indicated that genetics is the only presumed cause of ADHD; sited by 48% of the authors they investigated. However, no specific gene responsible for ADHD has as yet been isolated. There is evidence
that ADHD-type behaviours tend to recur in families (in first- and second-degree relatives of ADHD children (Barkley et al. 1990).
In a recent study, 55% of families presenting with an ADHD child had at least one parent with a lifetime diagnosis of ADHD. The frequency of ADHD in at least one
parent was higher in families with at least one affected girl than in families with only affected boys (Faraone, Biederman and Monuteaux, 2000/Smalley et al. 2000).
The gender sex difference in prevalence of ADHD is consistent in a model of inheritance in which girls require a greater loading of family influences to develop ADHD (Zametkin, 1995). The lack of familial clustering of ADHD suggests that hyperactive and inattentive symptoms reflect common familial underpinnings and not unique familial effects (Smalley et al. 2000).
A molecular genetic study suggests a possible relation to the D4 receptor gene (Levy, 1997). Increasing evidence suggests that ADHD is an inherited condition.
If one identical twin has symptoms of ADHD, the other twin has a 75 - 91% chance of sharing the same trait (Swanson, Lerner and Williams, 1995).
Children who have ADHD are likely to have one close relative who also has ADHD.
1/3 of all fathers who had ADHD when they were young have children who have ADHD (Swanson, Lerner and Williams, 1995).
Adoption studies provide evidence of a genetic link to ADHD: biological children of parents with ADHD have a far higher chance of having ADHD than adoptive children of parents with ADHD (Cantwell, 1996; Levy, 1997).
The parents of children with ADHD show an increased incidence of hyperkinesis, sociopathy, alcoholism and hysteria.
Monozygous twins are more alike than dizygous twins of same sex in measures of hyperactivity and inattention. Concordance for ADHD has been found to be much lower for half siblings than for full siblings, whether they are brought up by their mothers or are fostered (Kaplan and Sadock, 1988/Leary, 1994). These findings indicate that there may be a genetic link to ADHD.
Retrospective accounts suggest numerous congenital factors may be related to ADHD.
However, there is no compelling evidence for specificity of perinatal or congenital factors (Cantwell and Hanna, 1989).
Maternal substance abuse during pregnancy may be associated with ADHD (Engel et al, 1992). Substances such as cocaine and nicotine may induce ADHD-related symptoms (Holford, 2000).
These are very difficult to separate from genetic factors but the concept of parent and child temperament may be important (Tannock, 1998).
Several studies suggest that interaction between parents and children may lead to an exacerbation of predisposed attention deficit behaviour (Safer and Malever, 1995).
Hyperactivity and poor impulse control can also occur in response to significant familial stress. Children who have experienced a divorce, a move, and a change in school or other significant life events may display impulsive behaviour, forgetfulness and absentmindedness, which may be misdiagnosed as ADHD (Holford, 2001; Safer and Malever, 1995).
Parents of ADHD children have often been shown to be unresponsive to the child‘s demands. The child‘s hyperactivity may merely be an attempt to elicit a response from the parent (Biederman, 1996).
Children who have been active from birth are likely to remain so. The child‘s temperament and personality play an important part in the development of this ADHD (Biederman, 1996; Graham, 1986).
Central nervous system injury
One of the first theories was that minor head injuries or undetectable damage to the brain (due to early infection or birth complications) caused all attention disorders and learning disabilities. There has been no substantial evidence for this theory and thus it was dismissed (Tannock,. 1998).
Subtle brain damage may be found in some children that may result from circulatory, toxic, metabolic, or other disorders during critical periods of prenatal development.
In the early years of life, trauma, fever or inflammation can also cause subtle central nervous system (CNS) damage.
These stresses may cause a range of disorders such as cerebral palsy, seizure disorder, and mental retardation (Woods and Ploof, 1997). The less severe forms of damage
may produce a variety of learning disabilities including ADHD (Kaplan and Sadock, 1988; Tannock, 1998).
Environmental risk factors
While ADHD behaviours may be precipitated by deleterious social factors, with the exception of head injury occurring at a young age, there is no evidence of a single environmental agent causing ADHD (Paterson, 1999).
Feingold advocated foods containing additives, colourants and salicylates as the cause of ADHD in children (Feingold, 1973).
Although his diet has gained widespread popularity and offered an accessible alternative to ADHD management, numerous controlled studies have not yet validated his theory (Leary, 1994/Walker, 1983/Mattes and Gittelman, 1981).
Dietary supplements have been studied extensively over the last decade to understand the efficacy of dietary supplements for improving the symptoms of ADHD.
A number of these studies have found strong positive correlation between the use of certain supplements and ADHD (Schoenthaler, 2000).
In 1982, a conference was held to discuss the theory of what effect a restricted diet can have on the symptoms of ADHD. The data showed that the restricted diet only helped five percent of children with ADHD, and these were mostly young children or those with food allergies (Schoenthaler, 2000).
Refined Sugar and Food Additives
A later theory on the causes of ADD or ADHD suggested refined sugar and food additives attributed to making children hyperactive and inattentive (Holford, 2001).
This theory however was dismissed after it was found that there was no statistical validity for such a claim (Schoenthaler, 2000).
Colourants and Flavourings
The Lancet published a study in 1985, which reported that 79% of hyperactive children improved when certain foods were eliminated from their diets, only to become
worse again when the foods were reintroduced. Artificial colourings and flavourings were the most serious culprits; sugar was also found to have a noticeable effect.
Additives included: Artificial flavours and colour ants
Preservatives included: Butylated Hydroxyanisole (BHA) and Butylated Hydroxytoluene (BHT).
Sugars included: Sucrose, Fructose, Corn syrup, Mannitol, Sorbitol and other Sweeteners.
An experimental study done in New York confirmed that during a 4 year period, after eliminating food additives and colourants from t he diet, there was a marked increase
in academic performance in ADHD children (Schoenthaler et al. 1986).
Vitamin and mineral deficiencies have been implicated in mental performance (Muller, 1995).
Mineral status among those with ADHD has been the subject of several published clinical trials.
ADHD children are deficient in certain minerals (Holford, 2000).
These deficiencies can affect both behaviour and school performance. The effect of vitamin and mineral supplements on academic performance and children's behavioural problems is well documented and although it currently seems unlikely that ADHD is caused solely by nutrient deficiencies, addressing such deficiencies can significantly improve ADHD symptoms (Holford, 2002; Muller, 1995).
Magnesium Deficient Diets
Magnesium deficiency is the most common of the mineral deficiencies associated with ADHD (Starobrat-Hermelin, 1998).
In one study, magnesium deficiency was identified in 95% of ADHD children examined (Kozielec, 1997).
The conclusion from the investigations is that magnesium deficiency occurs more frequently in children with ADHD than in healthy children.
Analysis of the material indicated a correlation between increasing levels of magnesium and freedom from distractibility (Schoenthaler et al. 1998).
Iron plays a role in the regulation of dopaminergic activity (Schoenthaler and Bier, 2000).
The frequent occurrence of ̳restless leg syndrome‘ in children with ADHD may be associated with iron deficiencies (Sever et al. 1997). Some studies have shown
a clear relationship between low iron status and ADHD symptoms (Benton, Haller and Fordy, 1995).
Zinc is required for the conversion of essential fatty acids (EFA‘s) to prostaglandins (Black, 1998). In a recent study it was shown that zinc supplementation reduced the incidence of symptoms that with which ADHD children might present with (Stevens et al. 1995).
The Vitamin B-complexes includes all of the known essential water-soluble vitamins (except vitamin C), including thiamine (vitamin B1), riboflavin (vitamin B2),
niacin (vitamin B3), pantothenic acid (vitamin B5), pyridoxine (vitamin B6), biotin, folic acid and the cobalamins (vitamin B12).
For the management of ADHD symptoms, the B-vitamins work together in the brain for the production of the various neurotransmitters (dopamine, serotonin,
5-Hydroxytryptophan (5-HTP) and norepinephrine (Holford, 2001).
Vitamin B3 (Niacin/Nicotinamide)
Vitam in B3 is part of the vitamin B complex, which is considered by many to be the single most important set of factors needed for the body's proper maintenance
of the nervous system, proper functioning of cells and energy metabolism (Holford, 2002).
Niacin deficiency or imbalance plays a role in the symptoms of mood disorders.
Observational and experimental studies have shown an association between niacin and aggression, anxiety, ADHD, bipolar disorder and depression (Strohle,2003).
Clinical research has demonstrated that vitamin B3 supplementation may help to reduce peripheral breakdown of L-Tryptophan.
As a result, L-Tryptophan will not be used up for niacin production in the peripheral parts of the body, thus allowing it to be transported into the central nervous system
where it can be converted to serotonin (Holford, 2002).
It subsequently leads to an increased production of serotonin, a deficiency of which might lead to ADHD (Chouinard et al. 1999).
Vitamin B5 (Pantothenic Acid)
Pantothenic acid is responsible for helping to synthesize a neuro-chemical called Co-enzyme A (CoA) which combines with choline in the brain to produce the neurotransmitter Acetylcholine (Castellanos, 2000).
Although supplementation with pantothenic acid has not been proven as a treatment option for attention deficit disorder, it most definitely affects production of the neurotransmitter acetylcholine that may play a role in the development of ADD/ADHD (Holford, 2001).
In a recent clinical study involving older adults with cerebral disorders researchers found evidence that increasing levels of choline by way of supplementation helped to improve memory and cognitive function (Fioravanti et al. 2004).
Vitamin B6 (Pyridoxine)
The main function of pyridoxine is to convert amino acids into serotonin.
It forms an integral part in the metabolic pathway for the manufacture of brain chemicals, and an imbalance that can cause symptoms such as depression and ADHD
Vitamin B6 is an important coenzyme for the biosynthesis of neurotransmitters. These neurotransmitters are required for optimal brain functioning.
Researchers in Spain observed a clinical improvement in behaviour and school performance when patients were supplemented with vitamin B 6 and folic acid
(Fioravanti et al. 2004).
Vitamin B12 is essential for normal nervous system function and red blood cell production.
Scientists at Baylor University Medical Centre reported that vitamin B 12 and folic acid deficiencies could alter neurotransmitter function and contribute to neurologic and psychiatric pathologies (Fioravanti et al. 2004/Holford (2002) demonstrated that Vitamin B12 accelerates the learning process and is important for the health of the brain cells.
Folic acid has a protective function in the brain.
It protects the brain from chemicals like food additives and preservatives additives (Holford, 2002).
Assays of amino acid metabolism have generally revealed imbalances of these essential nutrients in ADHD. Serum amino acid levels as well as other nutrient cofactors may influence synthesis pathways for certain inhibitory and excitatory neurotransmitters (Kolesnichenko et al.1999).
Vitamin B6 is an important coenzyme for the biosynthesis of neurotransmitters.
These neurotransmitters are required for optimal brain functioning.
Researchers in Spain observed a clinical improvement in behaviour and school performance when patients were supplemented with vitamin B6 and folic acid (Fioravanti et al. 2004).
Vitamin B12 is essential for normal nervous system function and red blood cell production.
Scientists at Baylor University Medical Centre reported that vitamin B 12 and folic acid deficiencies could alter neurotransmitter function and contribute to neurologic and psychiatric pathologies
(Fioravanti et al. 2004).
Holford (2002) demonstrated that Vitamin B12 accelerates the learning process and is important for the health of the brain cells.
Folic acid has a protective function in the brain.
It protects the brain from chemicals like food additives and preservatives additives (Holford, 2002).
Assays of amino acid metabolism have generally revealed imbalances of these essential nutrients in ADHD. Serum amino acid levels as well as other nutrient cofactors may influence synthesis pathways for certain inhibitory and excitatory neurotransmitters (Kolesnichenko et al. 1999).
Research in the area of amino acids and ADHD points to a defect in metabolism o./+ synthesis of neurotransmitters.
Simply loading the amino acid precursors to neurotransmitters appears to be of limited clinical effect, perhaps owing to the failure of such therapies to address the und erlying errors of metabolism involved (Kolesnichenko et al. 1999).
Essential Fatty Acids (= EFA’s)
A deficiency in EFA‘s is being singled out by some as a cause of ADHD.
EFA‘s influence ADHD primarily in two ways: they influence gut permeability and are needed for the proper development of brain tissue (Burgess et al. 2000).
It is important to remember that a simple deficiency of EFA‘s due to decreased/insufficient intake is unlikely (Holford, 2003). Studies have shown that in many cases the child diagnosed with ADD/ADHD has siblings who are not affected, yet they adhere to the same basic diet (Middle borough, 2001).
There are three postulated reasons given for this deficiency:
a) ADD/ADHD children could have an inherent intestinal problem which leads to difficulty with absorption of EFA's.
A large-scale survey by the New York Institute for Childhood Development found that these children may be incapable of absorbing carbohydrates normally;, therefore a problem with fat absorption
would not be unlikely (Medical Hypothesis, 1981).
b) ADD/ADHD children could have a metabolic requirement for higher levels of EFA's than normal due to a genetic difference (Medical Hypothesis, 1981;
They fail to give close attention to detail, their work tends to be messy and they often make careless mistakes in schoolwork and other tasks.
ADHD individuals have great difficulty sustaining attention in tasks often shifting from one incomplete activity to another (Berkow et al. 1992).
They are easily distracted by irrelevant stimuli and frequently interrupt ongoing tasks to attend to trivial noises and events usually, and easily, ignored by others (American Psychiatric Association, 1991).
Impulsivity manifests as impatience, difficulty in delaying responses, frequently interrupting or intruding on others and making comments out of turn.
They may grab things from others and touch things they are not supposed to.
This picture often results in ADHD children being regarded as the - classroom clown.
They engage in reckless activities with little consideration of possible consequences (American Psychiatric Association, 1991).
They can exhibit overreaction to stress, have low frustration tolerance with catastrophic reactions of rage and outbursts, which subject them to continuous censure and rejection overtly or covertly (Breggin, 2001/Smith, 1983).
Hyperkinesis may be manifested by fidgetiness or squirming in one‘s seat, by excessive running or climbing in situations where it is inappropriate, or by talking excessively.
ADHD symptoms vary greatly with the individual‘s age and needs to be cautiously diagnosed, especially in toddlers and preschoolers, in whom symptoms can be variable and inconsistent (American Psychiatric Association, 1991).
Mood swings are common (Swanson, Lerner and Williams, 1995) and it is estimated that up to 25% of ADHD children suffer from depression (Berkow et al. 1992).
Wong (1985) found that 40% of children with learning disabilities scored in the depressed range on the Roberts Apperception Test for Children.
A study conducted in Los Angeles County over a three-year period found that 50% of the children under the age of fifteen who committed suicide had been identified as having a learning disability,
as compared to 5 – 8% in the general population (American Psychiatric Association, 1994/Peck, 1985).
DIAGNOSIS OF ADHD
Attention-deficit hyperactivity disorder (ADHD) is a common, heterogeneous disorder, conservatively estimated to affect 3% to 5% of school-age children (American Psychiatric Association, 1994/Anderson et al. 1987/Shaffer et al. 1996).
Attention Deficit Disorder (ADD) or Attention Deficit Hyperactivity Disorder (ADHD) is a collection of symptoms or criteria, rather than a true diagnostic entity (Borak, 2002).
There are no laboratory tests or specific features that have been established as diagnostic in the clinical assessment of ADHD (American Psychiatric Association, 1991).
Although ADHD is more prevalent in boys than in girls, little doubt exists that it is also an important cause of psychiatric disability in girls.
While the exact prevalence of the disorder in females remains unclear it may not be minor (American Psychiatric Association, 1991).
ADHD is a common psychiatric disorder that significantly hampers psychosocial adaptation (Biederman, 1996/Tannock, 1998).
Precise guidelines and criteria for the clinical diagnosis of ADHD in children are not universally accepted (Reichenburg-Ullman, 1996); this may account for the large variances in ADHD statistics in different countries.
In a trainee survey on residents at seven Ohio paediatric programmes it was found that 30% of children evaluated for ADHD were not given that diagnosis (the majority were considered to have
behavioural problems due to family dysfunction (Stancin et al.1990).
Further confusing the picture is that the concern the child raises in a social environment also varies according to family expectations and societal attitudes (NIH Consensus Statement, 1998).
Health care providers, such as paediatricians or child psychologists can diagnose ADHD with the help of standard guidelines from the American Academy of Paediatrics (DSM–IV-TR, 2000).
The diagnosis involves gathering information from several sources, including school, caregivers and parents.
The health care provider will consider how a child's behaviour compares with that of other children the same age.
The primary ADHD signs are behavioural and an accurate diagnosis is best made by an experienced health care professional.
Medical histories, school reports, rating scales, and checklists are essential for diagnosis (Mathews, 2000).
Due to the lack of specific organic signs in ADHD, if a diagnosis is made, it remains a clinical one (NIH Consensus Statement, 1998).
Minor physical anomalies such as hypertelorism (developmental defect characterised by an abnormally wide space between two organs or parts) (Glanze, 1986/Rapoport, 1995),
highly arched palate and low set ears, may occur at a higher rate than in the general population (American Psychiatric Association, 1991).
Waldrop and Goering (1971) found an increased incidence of head circumference out of the normal range in ADHD children. Also noted were higher rates of epicanthus (vertical fold
of skin from upper eyelid), widely spaced eyes, curved 5th finger, absence of ear lobes and widened spaces between the 1st and 2nd toes.
Soft Neurological Signs
On examination EEG abnormalities may be detected while neuropsychological testing sometimes shows non-localised soft neurological signs (minor neurological abnormalities) and
frontal lobe dysfunction (Sierles, 1993).
Neurological soft signs
(NSS) may be defined as minor abnormalities in the neurological examination in the absence of other features of fixed or transient neurological disorders (American Psychiatric Association, 1991).
Wender (1971) found an incidence of 50% of children suffering from ADHD to exhibit soft neurological signs such as:
Visual perception impairment
Auditory perceptual impairment
Poor motor co-ordination
Mild reflex asymmetries
Mild choreoform movements.
Neurological signs and minor physical anomalies cannot independently exclude or confirm a diagnosis of ADHD (NIH Consensus Statement, 1998).
Diagnostic and Statistical Manual of Mental Disorders Criteria
The DSM-IV classification has grouped two main symptom categories, firstly inattention and secondly hyperactivity/impulsiveness.
In each of the categories, six of the nine listed traits must be present for at least six months to warrant a diagnosis of ADHD.
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:
a) often fails to give close attention to details or makes 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 reluctant to engage in tasks that require sustained mental effort (such as schoolwork or homework)
g) often loses things necessary for tasks or activities (e.g. toys, school assignments, pencils, books or tools)
2) Six (or more) of the following symptoms of hyperactivity-impulsivity have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental evel.
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 (adolescents or adults, may be limited to subjective feelings of restlessness)
d) often has difficulty playing or engaging in leisure activities quietly and is often "on the go"
e) often acts as if "driven by a motor"
f) often talks excessively
g) often blurts out answers before questions have been completed
h) often has difficulty awaiting turn
i) often interrupts or intrudes on others (e.g. butts into conversations or games)
Some hyperactive-impulsive or inattentive symptoms that caused impairment were present before age 7 years.
Bullets and Numbering
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).
Because the criteria require symptoms to be present for at least six months in multiple settings, diagnosis of ADHD is not possible at a clinical visit, yet medical doctors promote the
idea of office diagnosis (Patricelli, 1994).
Because of the unreliability and subjectivity of measurement tools, no single objective measure can diagnose ADHD (McBurnett, Lahey and Pfiffner, 1993).
Assessment should include a network of parents and professionals using multiple methods in multiple situations, along with a thorough review of school records (Hunt, 1988; McKinney,
Montague and Hocutt, 1993).
Assessment instruments should be used to detect learning disabilities and emotional-behavioural disorders, which can co-occur with ADHD (McKinney, Montague and Hocutt, 1993).
Likewise, testing must include sensitivity to other DSM-IV disorders which may co-occur with ADHD, preclude a diagnosis of ADHD, or which need to be considered as alternative
explanations before a diagnosis of ADHD is made (DSM-IV).
Assessment Scales for ADHD Diagnosis
There are a number of assessment scales used to diagnose ADHD and measure the effectiveness of ADHD therapies such as the Conner's/CADS Scale, the Swanson, Kotkin, Atkins,
M-Flynn, and Pelham (SKAMP) scale, and Clinical Global Impression (CGI-I) scales.
Various Conner Rating Scales Revised (CRS-R)
versions offer flexible administration options while also providing the ability to collect varying perspectives on a child‘s behaviour from parents, teachers, caregivers and the child or
adolescent (NIH Consensus Statement, 1998).
There are three versions -parent, teacher and adolescent self-report- all of which also have a short and long form available. In addition, there are three screening tools that offer
the option of administering a 12-item ADHD Index or the 18-item DSM-IV
Symptom Checklist or both.
These instruments also offer versions for parents, teachers, and adolescents.
Two formats are included for self-report ratings and observer ratings.
Both the self-report and observer forms provide multimodal assessments of the same behaviours and problems and contain an identical set of scales, sub-scales and indexes.
Conner‘s Abbreviated Assessment Rating Scale (CAARS) forms are available in long, short, and screening versions.
Attentional difficulties and excessive motor activity are non-specific responses of the organism that can commonly be seen in completely unrelated disorders (Breggin, 2000).
The most common cause of these two symptoms in children can be anxiety or depression (Kaplan and Sadock, 1988/Tannock, 1998).
Attention Deficit Hyperactivity Disorder (ADHD), sometimes inaccurately referred to as ADD (there is no clinical term by this name) is a disorder usually first diagnosed in
infancy, childhood or adolescence (American Psychiatric Association, 1994/Holford, 2001/NIH Consensus Statement, 1998).
There are 4 recogniszed types of ADHD.
I. Predominantly Inattentive type;
II. Predominantly Hyperactive-Impulsive type;
III. Combined type (inattention and hyperactivity-impulsivity);
IV. ADHD- Not Otherwise Specified.
There is a high level of correlation between children with ADHD and other psychiatric illnesses. This includes illnesses ranging from behavioural, mood, family, anxiety, cognitive,
social to school functioning, with the greatest increase in those with the ADHD combined subtype (Fletcher, 1999).
ADHD needs to be distinguished from other learning disabilities such as environmentally based underachievement (e.g. children with anxiety, phobias, depression or other
psychiatric functional disorders) and mental retardation with uniform and broad deficiency in academic performance (American Psychiatric Association, 1991).
When an impulsive, inattentive and hyperactive child also exhibits considerable aggressive and antisocial behaviour, differentiation between conduct disorder and ADHD may be
difficult (NIH Consensus Statement, 1998).
Following is a brief outline of possible differential diagnosis‘s (Biederman, 1991):
Epidemiology: Associated Conditions
Language and Learning Disability (10 - 15%)
Usually less hyperactive and more inattention
(70% with tics have ADHD)
Oppositional Defiant Disorder (33% of ADHD patients)
Conduct Disorder (25 - 50% of ADHD patients)
Major Depression (20% of ADHD patients)
Anxiety Disorder (25% of ADHD patients) should not be diagnosed if presenting symptoms are better accounted for by other mental disorders such as:
Personality change due to general medication
Substance related disorders
Oppositional behaviour (American Psychiatric Association, 1991)
A misdiagnosis can easily be made in cases of suspected ADHD.
This has practical consequences because treatment with psychostimulants is contraindicated in most of the above mentioned disorders (Bazier, 2001/Breggin, 1999/Kaplan and Sadock, 1985).
Webb and Latimer (1993) discuss another condition which can complicate ADHD diagnosis: Giftedness.
Traits of gifted children which may lead to false ADHD diagnosis include off task behaviour, less need for sleep, questioning of rules and traditions, power struggles and resistance to repetitive tasks.
EVALUATION OF TREATMENT
Once a child has been diagnosed with ADHD, and the appropriate dose level for the prescribed drug has been identified, continued monitoring of response to treatment is essential. Several questionnaires
used in the initial evaluation can be completed regularly by the parent and teacher of the ADHD child to establish the degree of change in hyperactive behaviours (NIH Consensus Statement, 1998).
In addition to this, the child on the medication should have a follow-up clinical examination every 6 - 8 months.
During this time height, weight, blood pressure, and heart rate should be recorded to determine potential side effects (Biederman, 1996).
Current management of ADHD is multifactorial, often involving medication, behavioural counselling and dietary control.
For some children behavioural modification and educational support is sufficient. Some children require only one form of therapy to improve while others respond with a combination of therapies.
In some instances the parents of ADHD children can attend parent counselling. This supports the theory that ADHD is multifactorial (Breggin, 2000/Holford, 2001).
Cerebral stimulants are the most widely used drugs for the management of ADHD.
However, the results of several long-term follow-up studies have indicated minimal improvement beyond those obtained at the onset of treatment (Biederman, 1991/Breggin,1998).
It is still unclear whether stimulants do in fact improve long-term academic achievement (Breggin, 1999).
Children with ADHD do not outgrow their problems.
Therefore, long-term use of stimulants is often required needed, while of which the effects are limited in scope as well as in time (Whalen and Henker, 1991).
Behaviour modification is a technique used to modify behavioural patterns in children with ADHD.
According to Green and Chee (1997), the basic law of behaviour modification states:
"A behaviour which pays off for the child will be repeated - a behaviour that brings no advantage to the child will disappear.
This means that if the right behaviour is rewarded, it should happen more frequently, while ignoring what is undesired means it should disappear (Green and Chee 1997).
The key concepts of behaviour modification in the management of ADHD are immediacy and consistency in as many areas of the child's environment as possible (home, school and if possible,
during leisure activities) (Woods and Ploof, 1997).
These concepts must be present in all forms of behaviour modification.
As with other skills, consistency and immediacy need to be practiced and reinforced before they become automatic (Woods and Ploof, 1997).
The secret of behaviour modification is reinforcement with small, frequent rewards (Green and Chee, 1997).
To encourage the best behaviour, hard, soft or cumulative rewards can be used.
A hard reward is something tangible such as money, food or a special privilege.
Soft rewards are praise, enthusiasm or a show of parental pride.
Cumulative refers to the collection of stars, stamps or tokens, each given for a small period of good behaviour, and eventually adding up to a major prize (Green & Chee, 1997).
As the child learns acceptable behaviour, so the rewards should be gradually decreased (Warner-Rogers, 1998).
Parents and teachers need to initially give material rewards, along with praise, to reinforce appropriate behaviour and subsequently they may use praise alone to maintain the behaviour (Green and
Chee, 1997/Warner-Rogers, 1998).
Therefore rewarding positive behaviours not only reinforces that behaviour but also provides the child with desperately needed success, which in turn builds their self-esteem (Green and Chee, 1997).
The basic strategies for parenting a child with ADHD include:
a) providing a high degree of positive attention and consequently no complaining about bad behaviour
b) developing clear, concise and consistent expectations for behaviour;
c) utilising non-physical negative consequences for problem behaviours in a non-punitive fashion (Warner-Rogers, 1998).
A disorganised, unstable home environment can promote the development of symptoms more readily than one that is more structured and stable (Green and Chee, 1997).
If the parents can learn to become more organised and structured at home, the child with mild symptoms may make gains without medication.
The need for structure is substantially more important in the ADHD child who likes to have a fixed framework to direct their day.
They wake at a certain time, put their pyjamas under their pillow, straighten the duvet, get dressed, have breakfast, etc.
If their equilibrium is thrown by anything different their ADHD symptoms may worsen (Green and Chee, 1997).
Parents need to understand that the lack of a structured front within the home will only exacerbate the child's difficulties due, for example, to the obvious failure to provide needed
consistency (Green & Chee, 1997/Woods and Ploof, 1997).
An important aspect of behaviour modification is in communication.
Parents and teachers are advised to be very direct and explicit in communicating directions and feedback.
They should make eye-to-eye contact, use a clear, distinct voice and use simple terms.
This is often the only way to maintain the child's attention while relating significant information (Green and Chee, 1997/Woods and Ploof, 1997).
Parents and teachers are advised to exaggerate the level of praise for the child's behaviour even in academic tasks (Green and Chee, 1997/Woods and Ploof, 1997).
This is accomplished through the use of exaggerated facial expressions, gestures and an emotional tone of voice.
The benefits of an exaggerated praise approach are twofold.
First, it might help to activate the reinforcement systems of the brain.
Secondly, ADHD children have an almost constant need for personal attention because of the failure of their own reward and punishment systems, leaving them with an intense awareness of an
internal emptiness that can only be relieved through the overt expression of feeling from others (Green and Chee, 1997/Woods and Ploof, 1997).
Ness and Price (1990) believe that "the best non-medical interventions (for ADHD) are practical, common sense adjustments to an impulsive and disorganised style.
They also go on to state that those suffering from ADHD will be more frustrated, apathetic and pessimistic than others about psychosocial treatments, decreasing the probability of success.
Thus, the important first step in the treatment of a person with a learning disability is the gaining acquisition of their participation, and helping them to becoming active participants in their treatment.
Two of the first obstacles that must be overcame initially in order to do this are the common feelings of denial and under-confidence (Ness and Price, 1990).
According to Barton and Fuhrman (1994), the four problems that are brought into the therapeutic setting by the ADHD client are stress and anxiety resulting from struggles to meet life's demands,
low self-esteem, and feelings of incompetence, grief over lack of accomplishments and helplessness.
Another factor that can be added here is social skills.
Up to 20% of children and adults with ADHD will not respond to medications, and many more will experience only partial remission of their symptoms.
Additionally, a significant portion of the impairment from ADHD comes from or its secondary impact on self-esteem and social skills deficits.
These are the targets of psychotherapeutic interventions (Clinical Practice Guideline, 2001).
Another intervention that forms part of the multidisciplinary approach to ADHD is the work of occupational therapy.
The occupational therapist works on the child's sensorimotor skills through the use of tactile, kinaesthetic, motor planning and motor accuracy skills as well as verbal and visual cues (Kleinman and
This may include such simple skills as tying shoelaces, throwing a ball straight, catching a ball or moving smoothly (Green and Chee, 1997).
Their visual perception is targeted through the use of figure-ground discrimination, parts-to-whole-relationships and spatial relationships.
Their cognitive skills are enhanced with sequencing skills, number concepts and measuring skills (Kleinman and Stalcup, 1991).
Many ADHD children have problems with hand writing and it is the occupational therapist that helps with their pencil grip, organisation of letters and the flow from word to word (Green and
Occupational therapists work with children with Sensory Integration Dysfunction. They use sensory integration and recreational activities to build up their basic sensory and motor skills (Kranowitz,
Orthodox Pharmaceutical Intervention
Since medication is frequently used in the treatment of ADHD, it is important to have reasonable expectations regarding its effectiveness and to be aware of potential side effects.
(A) General Medication Information
Each person responds uniquely to medication.
Medications are very safe.
More studies have been done about on children taking stimulant medications than any other medications, including non-prescription drugs.
Medication should be prescribed in minimal doses.
Individuals do not have a physical craving for medication.
When medication is out of the blood stream, the individual goes back to exhibiting full-blown ADHD symptoms.
Both hyperactive and non-hyperactive individuals can benefit from medications.
Medication is effective for 54% of non-hyperactive children and 80 - 90% of hyperactive children.
Medication does not cause psychosis but can precipitate a psychosis in susceptible individuals (NIH Consensus Statement, 1998).
Medication Does Not:
Teach the ADHD individual how to cope and compensate for difficulties.
Imply a - magic pill".
Just treat hyperactivity. Medication also helps with impulsivity and attention difficulties.
Lead to aggressive, dangerous behaviour.
Cause seizures or Tourette‘s Syndrome (Karen et al. 1997/NIH Consensus Statement, 1998).
Treat ADHD symptoms.
Influence long-term progress and prognosis of ADHD children when utilised in conjunction with treatment modalities specific for ADHD.
Stimulate the attention centre of the brain to function more normally.
Affect impulsivity, attention, and behaviour positively. More specifically, stimulants can increase attention span, concentration, and compliance; improve handwriting and fine motor skills
and allow improved peer relationships.
In addition, a decrease in impulsivity, aggressiveness,and hyperactivity can occur. (Karen et al. 1997).
Many clinicians treating ADHD believe that greater harm - emotionally and socially occurs to untreated ADHD patients than could possibly come from the side effects of the medications.
Not everyone agrees, however, and many parents are concerned about the side-effects of medications.
Nevertheless, the usefulness of psychostimulants in the treatment of ADHD has been established and is the standard of care in mainstream medicine (Greenhill et al. 2002).
Stimulants have been widely prescribed by physicians for more than 40 years for a variety of disorders including Parkinsonism, depression, fatigue states, narcolepsy, asthma, obesity and
hyperactivity in children (Karen et al. 1997).
They are widely prescribed as adjuncts to other remedial measures (psychological, educational and social) in ADHD management. Stimulants should only be prescribed for ADHD after remedial
measures such as psychological and sociological intervention as well as appropriate educational placement have been proven to be insufficient alone (Borak, 2002).
There are many styles for the use of medication in ADHD.
Some clinicians increase the medicine's dose until the desired effect is achieved or too many undesirable side effects [jitteriness, stomach (aches) or headaches] occur and do not subside
after several weeks (Breggin, 1999/Holford, 2001).
Some clinicians use other medications to treat the side effects of the psychostimulants, an approach that becomes even more problematic for parents already concerned about the
consequences or long-term effects of medication use (Karen et al. 1997).
Mechanism of Action
The exact mechanism by which psychostimulants benefit ADHD children has not yet been identified.
They are known to facilitate dopamine and noradrenalin release by inhibiting the action of monoamine oxidase (MAO) (Leary, 1994/Lawson-Wending, 1981).
The calming action is non-specific and has been reported in normal children as well (Karen et al. 1997/Spencer et al. 1996).
Many controlled studies using both subjective and objective criteria to judge response, indicate that psychostimulants are beneficial in children with ADHD when used for one
to three months (Caroll and Rounsaville, 1993; Swanson et al. 1995). When properly prescribed, stimulants have a paradoxical calming effect on hyperactive children, and will
facilitate their educational and social development (Caroll and Rounsaville, 1993/Karen et al. 1997).
Stimulants have been shown to improve short-term learning by prolonging attention span; improving goal directed activity, concentration and classroom behaviour and reducing
impulsiveness, hyperactivity, and aggressive behaviour in children. The behaviour of treated children was found to be organised in a more efficient and effective manner, with
better processing of incoming stimuli and better planned responses (Frei et al.2001/Kaplan and Sadock, 1985/Karen et al. 1997).
Benefits were particularly seen in ratings of behavioural functioning, lowered activity levels, and improved attending skills (Levin and Kleber, 1995).
Side Effects and Contraindications
Side effects commonly seen include decreased appetite, insomnia, increased heart rate or blood pressure, stomach-aches (Holford, 2001), withdrawal symptoms and irritability
(Swansone al. 1991).
Long-term use of the psychostimulants may limit linear growth and weight, most likely due to appetite suppression, decreased food intake, and altered secretion of growth
hormone (Holford, 2001/Wilens et al. 1997). Children with a history of tics, Tourette's disorder, thought disorder, or psychosis should not receive stimulants as they have been
alleged to precipitate the symptoms of such disorders (Bazier, 2001/Breggin, 2000/Lowe, 1982).
Loss of spontaneity and apathetic withdrawal are signs of overdosage (Leary, 1994).
Special Prescriber‘s Points
Occasional - drug holidays‖ over weekends and holidays restores sensitivity to the stimulants and allows the dosage to be decreased when therapy is reinstated
(Caroll and Rounsaville, 1993/Swanson et al. 1995).
As many as 20% of children who respond poorly to one stimulant are believed to show a positive response to a second one.
It is generally recommended to begin stimulant medication with Ritalin®, followed by Cylert® if a poor response to Ritalin® develops (Karen et al. 1997).
Determining when it is safe to discontinue medication is a controversial topic. Barkley (1981) has found that as many as 26% of the children can discontinue the
medication because of improved self-control after two years of treatment.
He does state that this is not because the children are cured or have outgrown their disorder, but because their problems are not severe enough to warrant the continued use
Methylphenidate HCL (Ritalin®) and sustained-release preparations (Ritalin-SR®, Concerta®, Metadate CD®):
Methylphenidate is said to affect as much as a 70% improvement in those affected with ADHD.
Methylphenidate is supposed to induce hyper-perfusion [increase blood supply] to the frontal lobes of the brain (Greenhill et al. 2002). Of all the ADHD medications,
Ritalin® is the most inconsistently absorbed (Caroll and Rounsaville, 1993). Some adults and children absorb as much as 80 - 90% of the medication, whereas others only
absorb 30 - 40% of a medication dose (Karen et al. 1997).
Since 1990, prescriptions for Ritalin have increased by 500% in the USA (Holford, 2001/Breggin, 1999/Baizer, 2001/Wilens et al. 1997).
In South Africa there is considerable evidence that methylphenidate is being over prescribed (Cotton, 1988/Middleborough, 2001/Strauss, 2000).
Methylphenidate is derived from the same family as cocaine and increases blood flow to the basal ganglia and decreases flow to frontal and motoric regions (Bazier, 2001).
Cerebral studies in persons with ADHD have shown cerebral hypo-perfusion in the frontal lobe and decreased blood flow to the caudate nucleus (Zametkin and Rapoport, 1987).
Methylphenidate hydrochloride (Ritalin®), a piperidine derivative of amphetamine, is the drug of choice when it comes to stimulant treatment of ADHD children (Holford, 2002).
Mechanism of Action
The mode of action of methylphenidate hydrochloride in man is not completely understood, but methylphenidate presumably activates the brain stem arousal system and cortex
to produce its stimulant effect (Castellanos, 2000).
There is neither specific evidence that clearly establishes the mechanism whereby methylphenidate produces its mental and behavioural effects in children, nor conclusive evidence
regarding how these effects relate to the condition of the central nervous system (Spivak et al. 1999).
Methylphenidate hydrochloride in extended-release tablets is more slowly but as extensively absorbed as in the regular tablets (Karen et al. 1997).
Bioavailability of the methylphenidate hydrochloride extended-release tablet was compared to a sustained-release reference product and an immediate-release product (Karen et al. 1997/
MD Pharmaceutical Inc., 2002).
The extent of absorption for the three products was similar, and the rate of absorption of the two sustained-release products was not statistically different (Karen et al. 1997).
Methylphenidate is an indirectly acting sympathomimetic agent (a drug that stimulates the sympathetic nervous system) that releases dopamine and noradrenalin inhibits MAO
and probably acts directly on catecholamine and serotonin receptors (Spivak et al. 1999).
As compared to the other amphetamines, Ritalin acts more directly on dopamine release (Strohle, 2003/Zametkin and Rapoport, 1987).
In numerous comparative studies, Ritalin® proved to be statistically superior to dextroamphetamine (Dexedrine®) and magnesium pemoline (Cylert®) in several measurements
of improvement. Behavioural improvement appeared to be sustained for at least two years as judged by subjective criteria (Baizer, 2001/Paterson, 1999/Spivak et al. 1999).
Approximately 35 % of children with ADHD show a dramatic improvement on Ritalin®, while another 35% show only moderate improvement (Safer and Allen, 1976/Zametkin, 1995).
25 - 30% of children are poor responders and need alternative treatment (Leary, 1994/Berkow et al. 1992/Greenhill et al. 2002).
Methylphenidate has been reported to increase attentiveness, reduce distractibility, enhance concentration and decrease motor restlessness and hyperactivity in ADHD patients (Barkely
et al. 1990/Paterson, 1999).
Methylphenidate is reliably associated with a short-term enhancement in sustained attention, impulse control and reduced activity levels (Levin and Kleber, 1995/Strohle, 2003).
Positive behavioural effects include increased compliance, independent play and responsiveness to social interactions with parents, teachers (peers (Mino and Ohara, 1991/Whalen et a
However Buhrmester et al. (1992) found that stimulants had a general dampening effect on social behaviour, significantly reducing social engagement and increasing dysphoria
[an emotional state characterised by depression, restlessness, and malaise] (Greenhill et al. 2002).
Side Effects and Contraindications
Undesirable side effects such as nervousness, sleep disturbances, appetite suppression, anxiety, high blood pressure and headaches are common (Holford, 2001/Karen et al. 1997).
These side effects are largely dose dependant and spontaneously remit once the medication is discontinued (Karen et al. 1997/Levin and Kleber, 1995).
Prolonged therapy may result in anorexia, weight loss and growth retardation (South African Medicines Formulary, 1995). Decreased growth rates are only temporary. Once
the medication is stopped the child catches up with his peers with no long-term growth problems (Kozielec, 1997).
Less commonly seen side effects include dizziness, dyskinesia, rashes, nausea, abdominal pain, hypertension, hypotension, palpitation, tachycardia and arrhythmias, and headache.
(Holford, 2001; Breggin, 2000).
Induce hypersensitivity (including skin rash, urticaria, fever, arthralgia, exfoliative dermatitis, erythema multiforme with histopathological findings of necrotizing vasculitis, and
thrombocytopenic purpura); anorexia, nausea, dizziness, palpitations, headache, dyskinesia; drowsiness, blood pressure and pulse changes, both up and down;
tachycardia; angina; cardiac arrhythmia; abdominal pain; weight loss during prolonged therapy (Holford, 2002). Rare reports of Tourette's syndrome (Baizer, 2001).
The drug has also been shown to inhibit certain drug metabolising liver enzymes, causing a prolongation of the half-life of certain anti-epileptic drugs, tricyclic antidepressants
and MAO inhibitors (Karen et al. 1997).
This may result in an elevation of therapeutic doses to toxic levels.
Acute episodes of psychosis and hallucinations have been reported with Ritalin (Lambert and Hartsough, 1998/NIH Consensus Statement, 1998).
Methylphenidate is contraindicated in patients with marked anxiety, tension, thyrotoxicosis, tachyarrhythmias, agitation, or glaucoma.
Should be used cautiously in epileptic and hypertensive patients (Bazier, 2001/Karen et al. 1997).
Methylphenidate may decrease the hypotensive effect of guanethidine.
It should be used cautiously with pressor agents and MAO inhibitors.
Human pharmacologic studies have shown that methylphenidate may inhibit the metabolism of coumarin anticoagulants, anticonvulsants (phenobarbital, phenytoin, primidone),
phenylbutazone, and tricyclic anti-depressants (imipramine, clomipramnine, desipramine).
Downward dosage adjustments of these drugs may be required when given concomitantly with methylphenidate (Karen et al. 1997)
Special Prescriber‘s Points
Abuse and dependence on the amphetamine-type drugs (e.g., methylphenidate) are common (Clarke, 1986/Bazier, 2001).
Although there have been no reports of psychic dependence with methylphenidate use in ADHD children, the possibility for drug abuse needs to be acknowledged
(Barkley, DePaul and Connerors, 1999/Biederman, 1996).
A recent study showed that children with learning disabilities (including ADHD) display a higher proportion of chemically dependant traits when compared to children without any
learning disabilities (Karacostas, 1993).
Kavale (1985) completed an extensive review of the research done on the efficacy of methylphenidate in ADHD management.
He could not draw any conclusions on methylphenidate‘s benefit on ADHD.
This was mostly due to methodological flaws in studies completed on methylphenidate‘s efficacy (NIH Consensus Statement, 1998).
Long-term follow-up studies indicate that children on methylphenidate may continue to have difficulty in school, exhibit behavioural disorders and have poor self-esteem into
adolescence, which may persist as personality-trait disorders into adulthood (Bazier, 2001/Holford, 2001/Karacostas, 1993/Milman, 1979).
Pemoline (Cylert®): ranks third in sales for the treatment of ADHD (NIH Consensus Statement, 1998).
Unlike other stimulant medications, Cylert ® has an onset of action of about an hour and must be taken for 1-2 weeks before improvement occurs.
Cylert® is more expensive than Ritalin® or Dexedrine® (Bazier, 2001).
Important points about Cylert®:
Liver enzyme changes have occasionally been noted in patients taking Cylert®.
Baseline liver enzymes (tests?) are recommended with follow-ups at 3 – 6 months.
Persons using alcohol are at higher risk with this medication.
Patients with either liver or kidney compromise should not take this medication.
SSRI‘ (Selective Serotonin Reuptake Inhibitors) affect the use of Cylert® due to their effects on the liver P450 isoenzymes.
Cylert® is a useful alternative for patients with cardiovascular disease, as it has no effect on this system.
Cylert® may cause insomnia, appetite suppression, and tics (American Academy of Paediatrics Committee on Children with Disabilities, 1996; Bazier, 2001).
Mechanism of Action
Cylert® (Pemoline) has a pharmacological activity similar to that of other known central nervous system stimulants, however, it has minimal sympathomimetic effects.
Although studies indicate that Pemoline may act in animals through dopaminergic mechanisms, the exact mechanism and site of action of the drug in man is not known
(Spivak et al. 1999).
There is neither also no specific evidence, which clearly establishes the mechanism whereby Cylert® produces its mental and behavioural effects in children, nor conclusive evidence
regarding how these effects relate to the condition of the central nervous system (NIH Consensus Statement, 1998).
Pemoline (Cylert®) is metabolized by the liver.
Cylert® is excreted primarily by the kidneys with approximately 50% excreted unchanged and only minor fractions present as metabolites (Spivak et al. 1999).
Cylert ® (Pemoline) has a gradual onset of action. Using the recommended schedule of dosage titration, significant clinical benefit may not be evident until the 3rd of 4th week of
drug administration (Pelham et al. 2001).
Side Effects and Contraindications
Common adverse affects to Cylert® include insomnia, anorexia and weight loss (weight gain occurs after three to six months of continued administration). Less frequently occurring
side effects include dizziness, drowsiness, headache, depression, hallucinations, rashes, nausea and gastrointestinal distress (Karacostas, 1993/Pelham et al. 2001).
Most of these reactions were, however, reversible on withdrawal of the drug (Karacostas, 1993/Spivak et al. 1999).
Hepatic dysfunction has occurred in a few patients with elevated hepatic enzyme levels. One case of fatal hepatic dysfunction has been reported (NIH Consensus Statement, 1998).
Second-line Therapy - When Stimulants Cannot Be Used
Anti-depressant medication is often prescribed for persons with ADHD who cannot tolerate or show no signs of improvement on stimulants, or for those who have mood
sequealae (Karen et al. 1997).
Dosage levels, while there are guidelines, are essentially determined on a case-to-case basis.
Because ADHD persons are often poor self observers it may be helpful to enlist a person with whom the ADHD person is close in order to note any improvement or deterioration in
Behaviour following medication changes (Spivak et al. 1999).
It should be strongly emphasised that treatment of ADHD with anti-depressants does not necessarily imply that the patient is depressed.
Antidepressants are often used to enhance the control of the patient's symptoms, rather than as treatment of primary depression (Spivak et al. 1999).
Some clinicians feel that the SSR I's (Selective Serotonin Re-uptake Inhibitors) have superior benefits, especially with children, for the mooded aspects of ADHD because
they cause less side-effects than older generation anti-depressants such as the tricyclics (Imipramine®, Nortriptyline®, Amitryptyline®, Desipramine®).
Desipramine® has become less prescribed due to some unexplained sudden deaths which appeared to be related to heart conduction patterns (Bush et al. 1999).
Busiprone (BuSpar®) in Treating ADHD is a relatively new anti-anxiety medication which shows some promise in treating ADHD when psychostimulant medications are not effective
or their side effects cannot be tolerated (Bush et al. 1999/Spivak et al. 1999).
It can also "potentiate" benefits of the serotonergic antidepressants.
The side-effects of Busiprone are often tolerated better than those of other medications used for ADHD (Pelham et al. 2001).
It should always be remembered that, for reasons still not fully understood, every individual responds differently and uniquely to a specific medication. The effective administration of a specific medication for any psycho-neurological condition will still -and most likely will for quite some time- remain an art, rather than a science (Spivak et al. 1999).
Imipramine Tofranil® is a tricyclic antidepressant that has a marked sedative action in children.
Beneficial results however, have not been consistent (Pelham et al 2001).
These drugs should only be considered as alternatives in patients who cannot tolerate or do not respond to Dexedrine®, methylphenidate, and Cylert® (Karen et al. 1999).
Mechanism of Action
This drug acts pharmacologically by blocking the re-uptake of noradrenaline and serotonin into the presynaptic neuron and indirectly modifies their rate of release. To some extent,
it also inhibits dopamine re-uptake (McCracken, 1991).
Tricyclic antidepressants have been shown to effectively increase attentiveness and reduce distractibility in children and adults.
Tofranil® has been identified as being superior to a placebo in inducing school return and in global therapeutic efficacy in 40 - 85% of ADHD cases (Huessy and Wright, 1970/Karen et al. 1997/
Waizer et al. 1974/Wiener, 1977/Winsberg, et al. 1972).
It was found to decrease hyperactivity, aggression, defiance, and inattentiveness. In a comparative study between methylphenidate and Tofranil®, all rating measurements favoured Tofranil®
(Karacostas and Fisher, 1993/Wiener, 1977).
Other investigators have found that, although Tofranil® may initially control ADHD, thereafter the child‘s behaviour deteriorates over a 2 - 3 month period (Katzet al. 1975/Karen et al 1997/
Side Effects and Contraindications
The main side effects of Tofranil® include nausea, weight loss, insomnia, dry mouth, constipation, drowsiness, gastric upset and difficulty with micturition.
Syncope and seizures may be precipitated (South African Medicines Formulary, 1995).
Special Prescriber‘s Points
2 - 3 weeks of therapy are required in order to see a therapeutic response to the tricyclic antidepressants (Wiener, 1977).
Fluoxetine (Lorien®; Lilly-Fluoexetine®; Nuzak®; Prozak®) one of a group of new generation antidepressants, which selectively inhibits serotonin re-uptake (Karen et al. 1997).
Mechanism of Action
It selectively blocks serotonin re-uptake at the pre-synaptic neurons.
A positive response may only be seen after two to three weeks of continued therapy.
Side Effects and Contraindications
Common side effects include headache and gastrointestinal disturbances.
CNS effects include nervousness, drowsiness, and confusion.
Fluoxetine should be used with caution in patients with hepatic or renal impairment and epilepsy (Pelham et al. 2001).
Special Prescriber‘s Points
Safe-use in children has not been established (South African Medicines Formulary, 1995).
COMPLEMENTARY/ALTERNATIVE TREATMENTS FOR ADHD
Biochemical Tissue Salts
William Schuessler, a German physician, identified 12 different mineral salts in 1873 which are essential for human life. He postulated that the balance of these 12 mineral salts were essential
for building and maintaining health, and that they could also be used to treat disease (Boericke and Dewey, 1984).
The Schuessler system is based on 12 remedies prepared according to the homoeopathic law to D6 potency (1:1 000 000) (Goodwin, 1980).
According to Schuessler‘s theory, symptoms presented by an ADHD child are indicators of various mineral deficiencies.
Subsequently, administration of these minerals to the ADHD child should result in an improvement in his/her overall condition (Fisher, 1978).
A study conducted by Muller (1996) showed that mineral therapy was effective in decreasing the overall hyperactivity exhibited by an ADHD child.
She advocates the use of mineral therapy as alternative to cerebral stimulants (such as Ritalin®) in some cases, or as a reinforcing treatment in others (Muller et al. 1996).
With regards to brain function, Niacin has significant benefits in reversing schizophrenia.
As early as 1957 Dr. Humphrey Osmond and Dr. Abram Hoffer from Saskatchewan in Canada proved that supplementing with niacin normalised behaviour in those diagnosed
with schizophrenia. Dr. Hoffer, who has now treated over 5000 schizophrenic patients, claims an 80% success rate using niacin and other connector nutrients.
Niacin and niacinamide doubled the two-year recovery rates from this mental disease after just five weeks (Holford, 2002).
As one of the most well researched herbs, gingko has been shown to improve short-term and age related memory loss, slow thinking, depression, circulation and blood flow
directly to the brain (Holford, 2001).
A review of ten studies testing gingko‘s effects on people with circulation problems, carried out at the University of Limburg in the Netherlands, found significant improvement in
memory, concentration, energy and mood (Holford, 2003).
It appears that by increasing cerebral blood flow, and therefore oxygen and glucose utilisation, gingko offers relief of the presumed ―side effects‖ of aging and may offer
significant protection against their development (Crook et al. 1992).
In addition, experimental and clinical studies show that gingko increases the rate at which information is transmitted at the nerve cell. It has also been shown to normalise the
acetylcholine receptors in the hippocampus of aged animals, to increase cholinergic transmission and to address many of the other elements of Alzheimer‘s disease
(Cenacchi et al. 1993/Holford, 2001).
Although cobalamin, as vitamin B12 is technically termed, appears in all animal foods and can be manufactured by beneficial bacteria in the gastrointestinal tract, a deficiency
and its health consequences are never far away, especially in vegetarians (Holford, 2002).
Absorption depends entirely on a healthy intestinal supply of ―intrinsic factor which is a substance made in the stomach that latches onto B12 and draws it into the bloodstream.
With age we generate less and less intrinsic factor, one of the reasons anyone older than fifty is vulnerable to a deficiency (Fioravanti et al. 2004).
A broad range of emotional and cognitive abilities relies on an optimal amount of Vitamin B12. In cognition tests of elderly people, for instance, those who had the poorest
scores had the lowest blood measurements of cobalamin (Holford, 2002). People diagnosed with depression had low levels of cobalt, the mineral that forms the centre
of the vitamin B12 molecule.
Restoring a healthier blood concentration relieves symptoms of dementia and confusion for many people (Holford, 2001).
It also contributes to minimising the mental deterioration that occurs in AIDS.
Research at King‘s College Hospital and the Institute of Psychiatry in London found that a third of all patients with either severe depression or schizophrenia were deficient in
folic acid (Fioravanti et al. 2004). Supplementing folic acid for six months made a big difference in their symptoms and ability to relate (Holford, 2002).
Folic acid, together with B12, is needed to convert the amino acid L-tryptophan into serotonin and tyrosine into dopamine (Holford, 2002).
Pantothenic acid (vitamin B5) is essential to convert choline, such as phosphatidylcholine, into the neurotransmitter acetylcholine, the key memory molecule (Holford, 2002).
Without this vitamin, supplementation of choline of any kind would be of little value (Engel et al. 1992).
Pantothenic acid is involved in the breakdown of carbohydrates, fats and protein and in the production of various enzymes, pantothenic acid is needed by the adrenal cortex for
the secretion of glucocorticoids (Fioravanti et al. 2004).
Pyroglutamate (2-oxo-pyrolidone carboxylic acid, or PCA) is an amino acid found in vegetables, fruits, dairy products and meats (Holford, 2001).
Arginine is a non-essential amino acid and is abundant in protamines and histones, which are both proteins associated with nucleic acids and was first isolated in 1895 from
animal horn 100 (Kolesnichenko et al. 1999/Murray et al. 1998).
Pyroglutamate is also present in large amounts in the human brain, cerebrospinal fluid and blood (De Freudis, 1998).
A key brain chemical in enhancing memory and mental function is the amino acid pyroglutamate and its derivatives.
Being on the receptor end of brain communication, pyroglutamate improves learning, memory, concentration and the speed of reflexes (Holford, 2002).
Pyroglutamate is known to have a number of remarkable cognitive-enhancing effects (Holford, 2002).
Toxicity and symptoms of high intake of Pyroglutamate: Although rare, but symptoms of massive dosages may include skin thickening and coarsening of the skin, weakness,
diarrhoea, nausea, as well as increasing the activity of some viruses.
For this reason people suffering from herpes should avoid high dosages.
Pregnant and lactating women and people suffering from schizophrenia should also avoid high dosages (Kolesnichenko et al. 1999).
So-called ―smart drugs‖ have been developed based on slight variations of this substance helping with learning and memory related problems (Borak, 2002; Holford 2001).
Numerous studies using these ―smart drugs‖ have proven to enhance memory and mental function, not only in those with pronounced memory-decline but also people with
so-called normal memory function (Blokland et al. 1999).
Although orthodox treatment may improve many aspects of general behaviour in the ADHD child, studies have failed to show it to be effective in improving school achievement
(NIH Consensus Statement, 1998).
Prognosis remains unchanged, whether the child is on allopathic drugs or no medication (Karen et al. 1993/Safer and Allen, 1976).
Follow-up studies on children with ADHD have found that they do not grow out of their difficulties (Biederman, 1996/Bird, 1996).
Long-term studies on ADHD children have indicated that only about 25% of these children make good adjustments to adult life. Approximately 15% of ADHD children become
psychotic at some stage during their adult lives and 40 - 60% continue to have significant concentration and impulse control difficulties (Borak, 2002/Leary, 1994).
Although ADHD is primarily regarded as a childhood disorder, it is, however, being increasingly identified that children with ADHD grow up to experience various
psychological problems such as chronic depression, drug dependencies and antisocial behaviour (Klein and Mannuza, 1991).
Morrison (1980) found an increased incidence of violence and legal problems, less education and low work status in adults who were diagnosed as suffering from ADHD
Subsequently Leary (1994) found that adolescents (with a history of ADHD) showed increased aggressive behaviour and conduct disorder and as adults. He found a higher
incidence of substance abuse, court summonses and involvement in motor vehicle accidents (Leary, 1994).
ADHD problems that may persist into adolescence and adulthood may manifest as
ulsiveness and attention deficiency
Mood and anxiety disorders
n and irritability (Haislip, 1996)
Drug use disorders
Antisocial personality disorders (25
) (Sierles, 1993).
ADHD is a socially and academically debilitating condition seen in 10 - 20% of school-aged children.
Inability to maintain concentration in the classroom environment is an important factor resulting in academic maladjustment.
It has been shown that ADHD is not primarily a childhood disorder and that symptoms do persist into adulthood (Strauss, 2000).
Ritalin®, the drug of choice, is effective in improving concentration, memory, frustration and anger, but it is ineffective in up to 30% of suffers (Picton, 1997).
Ritalin®, which physicians consider to have only short-term effects, may initiate changes in the brain structure and function that remain after the therapeutic effects have dissipated
Methylphenidate does not make a difference in the long-term outcome of ADD/ADHD (Breggin, 2001/Holford, 2001).
A recent study carried out at Montreal Children‘s Hospital discovered that at the end of five years, hyperkinetic children who received stimulant drugs (Ritalin® or Chlorpromazine®)
did not differ significantly from children who had not received these drugs (Karen et al. 1997).
Although it appeared that hyperactive children treated with Ritalin® were initially more manageable, the degree of improvement and emotional adjustment was essentially identical at
the end of five years to that seen in a group of children who had received no medication at all (Breggin, 2002/Holford, 2001).
Present drug management involves the long-term use of powerful drugs which can lead to dependency, whilst the long-term effects are not yet conclusive. There is no data to conclusively
demonstrate that these drugs improve learning over long periods (NIH Consensus Statement, 1998).
Many parents are dissatisfied with the use of drug therapy due to the adverse side-effects and lack of clinical response, and are thus therefore seeking alternatives (Whalen and Henker, 1991/
7 - 10% of the children in America take some form of psychostimulants at some point in their school career (Breggin, 2000; Holford, 2002). Data has shown a 1000% increase in drug
abuse injury reports involving Ritalin in the 10 - 14 year age group (Haislip, 1996).
Homoeopathy provides an alternative for many people seeking medication without fear of dependency or undesirable side effects. Homoeopathic remedies have minimal to no side
effects, should not produce dependency and are considered safe to use for all age groups (Jouanny, 1993).
A homoeopathic alternative to drug therapy in ADHD has not yet been extensively researched and may provide a relatively inexpensive and safe substitute to drug therapy.
Advanced Brain Food® is a nutritional supplement formulated to meet the needs of children with learning, concentration and behavioural difficulties. According to research
done by Holford in the United Kingdom (1998), the individual nutrients in Advanced Brain Food® have been shown to enhance neurologic function and learning capabilities as well as
assisting in moderating blood sugar changes.
This combination of nutrients offers the perfect solution in assuring that children receive the appropriate nutrients essential for growth (Holford, 2000).
The aim of the study was to evaluate the efficacy of the homoeopathic combination preparation Quietude® and a nutritional supplement, Advanced Brain Food® in the management of
ADHD in children. This study proposes to show that Quietude® +/o. Advanced Brain Food® could be used as an alternative to methylphenidate hydrochloride or other orthodox drugs
in the management of ADHD, with particular regard to concentration abilities, hyperactivity and impulsivity.
Subjects taking Advanced Brain Food® during the trial performed better than the group taking Quietude® with regards to conduct and impulsivity according to the Student
Behaviour Log (SBL), with a significant difference\between groups only being noticeable after four weeks of treatment. The groups performed similarly regarding inattention, hyperactivity
and anxiety (no significant differences were seen at the four different assessment periods).
Supplementation and treatment with Advanced Brain Food® cannot claim to replace effective psychological interventions but merely help to correct deficiencies. The fact
that an improvement was noted in this treatment group signifies that further research is necessary to establish the exact role of such interventions in the treatment of ADD/ADHD.
Hyoscyamus niger 3C HPUS (contains less than 10-9 mg alkaloids per dose) - Relieves restless sleep associated with nervousness
Nux moschata 4C HPUS - Relieves restless sleep
Passiflora incarnata 3X HPUS - Relieves sleeplessness associated with worries and exhaustion
Stramonium 6X HPUS (contains less than 10-8 mg alkaloids per dose) - Relieves sleeplessness with intermittent awakening
Advanced Brain Food®
Optimum Nutrition Formula Tablets (per daily intake 2 tablets)
Lithothamnion Calcareum, Calcium Citrate, Calcium Ascorbate (Preparation with Hydroxypropyl Methylcellulose),
Magnesium Oxide, Magnesium Citrate, Magnesium Ascorbate:
Providing Vitamin C
Vitamin E 135 i.u. (as D-Alpha Tocopheryl Succinate1)
Anti-Caking Agents (Magnesium Stearate, Stearic Acid & Silicon Dioxide)
Pantothenic Acid (Vitamin B5 as Calcium Pantothenate)
Niacin (Vitamin B3 as Nicotinamide)
Iron (as Amino Acid Chelate)
Choline (as Bitartrate)
Thiamine (Vitamin B1 as Thiamine Hydrochloride)
Zinc (as Citrate)
Riboflavin (Vitamin B2)
Tablet Coating (Hydroxypropyl Methylcellulose)
Vitamin B6 (as Pyridoxine Hydrochloride / Pyridoxyl-5-Phosphate)
Vitamin A 5000 i.u. (as Acetate with Acacia Gum, DL Alpha Tocopherol, Sucrose & Tricalcium Phosphate)
Boron (as Amino Acid Chelate)
Vitamin D 600 i.u. (Preparation as Ergocalciferol with Maltodextrin, Hydroxypropyl Methylcellulose & Tocopherols)
Manganese (as Citrate)
Biotin (Preparation with Dicalcium Phosphate)
Selenium (Preparation as L-Selenomethionine with Dicalcium Phosphate)
Iodine (Preparation as Potasssium Iodide with Dicalcium Phosphate)
Beta Carotene (Preparation with Alginate & Soya Protein1)
Vitamin B12 (Preparation as Cyanocobalamin with Dicalcium Phosphate)
Folic Acid (Preparation with Dicalcium Phosphate)
Vanadium (as Sulphate)
Vitamin K (Preparation with Acacia Gum & Sucrose)
Molybdenum (as Molybedenum Amino Acid Chelate)
Chromium (as Polynicotinate)
Copper (as Citrate)
Immune C (per daily intake 2 tablets)
Black Elderberry Extract (4% total flavonoids)
Bilberry Extract (2% anthocyanadins)
Essential Omegas (per daily intake 2 capsules)
Fish Oil providing EPA
Borage Oil providing GLA
Brain Food (per daily intake 2 capsules)
Pantothenic Acid (Vitamin B5)
Niacin (vitamin B3)
ADHS – eine fabrizierte Erkrankung?
Schreiende und tobende Kinder außer Rand und Band, verzweifelte Eltern, ohnmächtige Pädagogen: Keine andere Erkrankung des Kindes- und Jugendalters rückte in der Vergangenheit so stark in den Fokus der breiten Öffentlichkeit wie das sogenannte Aufmerksamkeitsdefizit-/Hyperaktivitätssyndrom, kurz ADHS.
Eine wahre Flut an ADHS-Diagnosen brachte das Fass vor einigen Jahren endgültig zum Überlaufen und erste kritische Psychiater und Psychotherapeuten meldeten sich zu Wort. Sie bemängelten nicht
nur die inkonsistenten Diagnosekriterien, sondern vermuteten auch einen nicht unerheblichen Anteil an Fehldiagnosen.
Damit lagen sie höchstwahrscheinlich richtig, denn Forscher der Ruhr-Universität Bochum konnten zeigen, dass es häufig zu Fehldiagnosen aufgrund der von Kinder- und Jugendpsychotherapeuten benutzten Faustregeln kommt. Die Experten verwenden zur Diagnosestellung also eher Heuristiken, anstatt sich an wissenschaftlichen Kriterien zu orientieren.
In einer weiteren Studie der Universität Köln legten die Forscher dar, dass auch ein Großteil der nicht an ADHS leidenden Jungen in bestimmten Entwicklungsphasen einzelne ADHS-Symptome zeigt, wodurch eine klare Differenzierung von der Norm noch erheblich erschwert wird.
Der „wissenschaftliche Vater“ des ADHS, der amerikanische Kinderpsychiater Leon Eisenberg, sprach 2009 von einem „Paradebeispiel für eine fabrizierte Krankheit“. Im Zuge dieser Kritik bezeichneten wichtige Wortführer ADHS als „gesellschaftliches Konstrukt“. Die Symptomatik wird dabei als Folge der aktuellen Lebensumstände verstanden, was gerade vielen Pädagogen aus dem Herzen spricht. Auch Eisenberg hatte kurz vor seinem Tod angemerkt, dass „die genetische Veranlagung für ADHS vollkommen überschätzt wird“ und „psychosozialen Aspekten mehr Beachtung geschenkt werden sollte“.
ADHS – eine gekaufte Diagnose?
Das Thema ist noch aus einem weiteren Grund so brenzlig, denn mit der Diagnose ADHS wird sehr viel Geld verdient: Das Nürnberger Pharmaunternehmen Novartis, welches das Medikament Ritalin herstellt, machte damit im Jahr 2010 einen weltweiten Umsatz von 464 Millionen US-Dollar.
Nach der Neuauflage des Diagnose-Handbuchs der American Psychiatric Association kam ans Licht, dass mehr als die Hälfte der Autoren der ADHS-relevanten Kapitel Einkünfte von der Pharmaindustrie erhielt. Neben Novartis und weiteren Pharmaunternehmen verdient am ADHS eine ganze Industrie, die Literatur, spezielles Spielzeug und weitere Produkte an die Eltern betroffener Kinder vertreibt.
Doch selbst wenn die genetischen Veranlagungen nur eine untergeordnete Rolle bei der Genese des ADHS spielen sollten und die Pharmaindustrie bei der Verbreitung der populären Diagnose kräftig mitmischte, so bleibt dennoch ein hoher Leidensdruck bei den betroffenen Kindern und die Ohnmacht ihrer Eltern und Betreuer, denn die Verhaltensauffälligkeiten sind, kulturelles Phänomen hin oder
her, durchaus real.
Es ist nicht zielführend, dem ADHS seinen Stellenwert als Erkrankung abzusprechen und zu glauben, dass damit alle Probleme vom Tisch seien. Aktuell wird die Debatte auf dem Rücken der
Betroffenen ausgetragen, anstatt nach möglichen Lösungsansätzen zu suchen.
Von Anfang an standen, vor allem bei den Praktikern, bestimmte Ernährungsfaktoren im Verdacht, ADHS auszulösen bzw. dessen Symptome zu verstärken. Doch auch die wissenschaftliche Forschung widmete sich diesem brisanten Thema, welches immer wieder zu hitzigen Diskussionen führte.
Erste ernährungstherapeutische Ansätze
In den 1970er-Jahren entwickelte Dr. Ben Feingold, ein amerikanischer Kinderarzt und Allergologe, erstmals eine spezielle Diät zur Behandlung von ADHS-Symptomen. Die Methode beruht auf der Vermeidung von synthetischen Zusatzstoffen (Farb-, Geschmacks- und Konservierungsstoffe) sowie von synthetischen Süßstoffen (z.B. Aspartam). Erste Studien mit oft geringen Teilnehmerzahlen berichteten Erfolgsquoten von teilweise über 70% und rückten Dr. Feingolds Ansatz in den Fokus weiterer Forscher. Doch leider waren die Ergebnisse der folgenden Untersuchungen bei Weitem nicht so beeindruckend, wie die faszinierenden Fallberichte. Die Diät half also einzelnen Kindern auf ganz erstaunliche Weise und einige konnten sich sogar ihrer Medikamente entledigen. Doch dem größeren Teil konnte nicht geholfen werden.
Trotz des eher enttäuschenden Fazits konnten durch die durchgeführten Folgeuntersuchungen einige neue Erkenntnisse gewonnen werden. Die wissenschaftlichen Publikationen zu Feingolds Diätansatz gingen aber über die Jahre konstant zurück.
Interessanterweise schaltete sich 1974 die Nutrition Foundation of New York in die Diskussion ein, eine Organisation, der u.a. Coca Cola angehörte. Obwohl sie ebenfalls weitere Untersuchungen angekündigt hatte, erklärte die Nutrition Foundation schon wenige Tage später, dass es „keine Hinweise aus kontrollierten Studien gäbe, die auf einen Zusammenhang zwischen künstlichen Zusatzstoffen und Hyperaktivität schließen lassen“. Dieser Satz wurde lange und oft von den Medien wiederholt und bekam dadurch leider für viele Eltern, aber auch zahlreiche Ärzte und Wissenschaftler, einen Wahrheitswert.
Im Jahr 2007 griff ein britisches Forscherteam die Ideen von Dr. Feingold auf. Die Wissenschaftler untersuchten 300 Kinder ihrer Gemeinde. Ein Teil der Kinder bekam ein Getränk, welches synthetische Zusätze in Form von Farb- und Konservierungsstoffen enthielt, während der Rest nur eine Placebolösung trank. Die Kinder, welche die Zusatzstoffe konsumierten, wurden in den Urteilen von Eltern, Lehrern und zusätzlichen unabhängigen Beobachtern als deutlich hyperaktiver eingeschätzt. Die Art und Dosis der synthetischen Zusatzstoffe findet sich regulär in zahlreichen, vor allem bunten, „Kinderlebensmitteln“.
Doch die britischen Forscher ließen es damit nicht beruhen. 2010 publizierten sie einen Artikel, in dem sie sich mit der Genetik jener Kinder beschäftigten, welche in der Southampton- Studie besonders hyperaktiv reagiert hatten. Sie konnten dadurch nachweisen, dass diese Kinder Probleme mit der Regulation ihres Histaminhaushalts hatten. Es scheint also, als sei ADHS in vielen (aber nicht allen) Fällen eine Folge einer Lebensmittelallergie.
Spätestens die Publikationen dieser neuen Befunde sollten dem oben zitierten Fazit der Nutrition Foundation of New York den finalen Streich versetzen.
Die bahnbrechende INCA-Studie
Belgische Wissenschaftler, welche sich 2011 der Verbindung zwischen Ernährung und ADHS widmeten. Sie untersuchten insgesamt 100 Kinder, welche bereits in der Vergangenheit eine ADHS-Diagnose erhalten hatten. Die jungen Probanden aßen über 9 Wochen eine sogenannte Eliminationsdiät (weißer Reis, Fleisch, Gemüse und Birnen) oder eine „gesunde Kontrolldiät“ (u.a. Vollkorngetreide, Pflanzenöle, Milchprodukte, Nüsse und Samen, Obst und Gemüse). Ziel der Eliminationsdiät war es, alle Lebensmittel mit potenziell allergenen Eigenschaften aus dem Speiseplan der Kinder zu verbannen.
Die Ergebnisse der Studie waren im wahrsten Sinne des Wortes beeindruckend: Etwa 60% der Kinder zeigten mit der Eliminationsdiät enorme Fortschritte bei den ADHS-relevanten Verhaltensauffälligkeiten. Diese Fortschritte verschwanden, sobald sie wieder zu einer „gesunden Kontrolldiät“ zurückkehrten.
(Es gab auch eine „sanftere“ Form der Eliminationsdiät, welche geringe Mengen Getreide beinhaltete. Doch nach zwei Wochen hatten 41% der Kinder überhaupt keine Reaktion auf diesen Ansatz gezeigt und wurden somit der eigentlichen Eliminationsdiät zugeordnet.)
Der negative Einfluss von vor allem glutenhaltigem Getreide auf die Verbesserung der Symptome scheint nicht wirklich verwunderlich. So zeigten zahlreiche Studien in der Vergangenheit mögliche Zusammenhänge zwischen Weizen und Schizophrenie, den depressiven Störungen und Autismus.
Neben den eigentlichen diätetischen Ansätzen gerieten in den letzten Jahren auch einige Mikronährstoffe in den Fokus der Wissenschaftler. Es wurde u.a. festgestellt, dass die Konzentration von langkettigen Omega-3-Fettsäuren in den Zellmembranen von ADHS-Betroffenen dauerhaft herabgesetzt ist. In der sogenannten Oxford-Durham-Studie erhielten Kinder mit Koordinationsproblemen ein Supplement mit einer hohen Omega-3- Konzentration. Die meisten Kinder zeigten eine deutliche Verbesserung der ADHS-Symptome, während die Kinder der Kontrollgruppe keine signifikante Linderung erfuhren. Auch die Buchstabier- und Lesefähigkeit verbesserte sich weitaus deutlicher in der Supplementgruppe.
In weiteren Studien konnte gezeigt werden, dass Kinder mit einem Zinkmangel mehr hyperaktives Verhalten zeigen. Eine Supplementation mit Zink ließ die benötigte Medikamentenmenge im Gegensatz zur Kontrollgruppe um ca. 30% sinken.
Des Teufels liebster Dämon? Der Zucker ...
Zucker stand schon frühzeitig bei Praktikern und Eltern im Verdacht, der Hauptschuldige am ADHS-Dilemma zu sein. Im Zuge der ersten Veröffentlichungen entspann sich eine der hitzigsten Debatten im Zusammenhang mit Ernährung und ADHS. Die gesammelten Erfahrungen tausender Eltern und Lehrer standen den statistischen Daten einiger Forschergruppen gegenüber. Zahlreiche Wissenschaftler verwiesen immer wieder darauf, dass Zucker in den durchgeführten Studien niemals konsistent zu aggressiverem oder hyperaktiverem Verhalten gegenüber Placebo geführt hatte.
Allerdings zeigen Kinder signifikante Änderungen im Elektroenzephalogramm und im Verhalten, wenn ihre Blutzuckerwerte rapide unter 75 mg/dl fallen. Dieses Phänomen, auch reaktive Hypoglykämie genannt, kann leicht durch eine zuckerreiche Mahlzeit provoziert werden. Es treten hierbei die für die Hypoglykämie typischen zentralnervösen Symptome auf, wie etwa Verwirrtheit, Konzentrationsund Koordinationsstörungen.
In einem wahren Mammutprojekt wurden Daten von über einer Million Schülern an öffentlichen New Yorker Schulen über sieben Jahre erfasst. Dabei wurde der Zuckerkonsum dieser Kinder stark reduziert und einige synthetische Farbstoffe aus der Ernährung verbannt, woraufhin sich die schulischen Testleistungen bedeutend verbesserten.
Weitere Unterstützung für die Eltern kommt durch Studien der Universitäten in South Carolina und Yale. Umso höher die zugeführte Menge an Zucker in den Untersuchungen mit ADHS-Kindern wurde, desto häufiger zeigten sie zerstörerisches bzw. aggressives Verhalten und Ruhelosigkeit. Auch der Grad der Unaufmerksamkeit stieg mit höherer Dosis an.
Ein weiteres Problem mit dem Zucker sind die vielen leeren Kalorien, welche dieser liefert. Mit anwachsendem Zuckerkonsum kommt es häufig zu einer mangelnden Zufuhr essenzieller Mikronährstoffe, u.a. auch den für die ADHS-Symptomatik so wichtigen Omega-3-Fettsäuren.
Ein Fazit und die brennende Frage: Was ist zu tun?
Dieser riesige Berg an Forschungsergebnissen scheint beinahe erdrückend. Doch nach dem Ordnen der Ergebnisse und Gedanken sollte eindeutig die Hoffnung überwiegen, dass eine Ernährungsumstellung vielen ADHS-Betroffenen helfen kann, ihre Symptome deutlich zu reduzieren – ganz ohne chemische Medikamente mit teilweise verheerenden Nebenwirkungen. Doch wo sollten Therapeuten und interessierte Eltern beginnen?
Inzwischen behandeln viele ADHS-Experten ihre Klienten mit Mischformen der oben vorgestellten Ansätze und das teilweise mit durchschlagendem Erfolg! Dr. Sandy Newmark z.B. empfiehlt eine zuckerarme Diät basierend auf unveränderten Lebensmitteln und unter Einbeziehung von Fischöl (Omega-3-Lieferant) und Zink.
Eine Weiterentwicklung der Specific Carbohydrate Diet, einer Diät zur Behandlung chronisch entzündlicher Darmkrankheiten, die sogenannte Gut and Psychology Syndrome Diet (GAPS), führt als eine Hauptindikation ADHS auf.
Entwickelt bzw. weiterentwickelt wurde dieser Diätansatz von Dr. Natasha Campbell-McBride. Interessanterweise eliminiert die GAPS-Diet alle gängigen und oben erwähnten negativen Einflussfaktoren, obwohl sie zeitlich vor den bedeutenden aktuellen Untersuchungen konzipiert wurde.
GAPS beruht auf unverarbeiteten Lebensmitteln, vor allem Gemüse, Obst, Nüssen und Samen, Olivenöl, Seefisch, Fleisch und Eiern. Der Diätansatz ist frei von Zucker und Getreide und liefert durch den Verzehr von fettem Seefisch wichtige Omega-3-Fettsäuren.
Obwohl zur Effektivität von GAPS in Bezug auf ADHS nur Fallberichte und keine klinischen Studien existieren, scheinen die oben aufgeführten Untersuchungen den Nutzen dieser Diät zu unterstreichen. Als besonders positiv kann natürlich auch das Vorhandensein von Literatur, Rezepten usw. gesehen werden, was den Einstieg und die praktische Umsetzung einer solchen Diät erheblich erleichtern kann.