A Brief History of Attention Deficiency Hyper-Activity Disorder Treatment, Literature Review Example
Words: 6069Literature Review
ADD and AHDH are acronyms for attention deficit disorder and attention deficit hyperactivity disorder. Attention Deficiency Hyper-activity Disorder (ADHD) is a multifaceted symptomatic condition that exhibits a range of abnormality features. Since treatment of the disorder(s) is not limited to address of a particular symptom, no single treatment therapy has proved absolute in effectiveness. Like most psychological and mental related disorders, manifestation of ADHD does not occur in a readily predictable manner. In general, the historical analysis of the condition has been shrouded in complex etiological literature; challenging singular diagnostic approach.
The use of alternative medicine in the treatment of ADHD coincides with the historical emergence of an etiological diagnosis of the phenomenon as a ‘disorder’ in the early 1970s. Alternative therapeutic interventions continue to be in high demand today, and augmentation of traditional medical intervention is widely sought by families and professionals looking for comprehensive approaches to behavioral management beyond drug therapy (Schab & Trinh, 2004). In recent years, interest has heightened even further in response to controversial, and near epidemic-proportion use of stimulants in children. According to National Institute of Health (NIH) (2000), the use of stimulant drugs toward reduction of hyperkinesis and attendant diagnoses has risen exponentially as parents search for remedy to hyperactivity in children. One factor for the increase is one of longitudinal research and a standard of care that focuses on lifelong treatment for disorders that are seen as chronic, so that more elementary school children are remaining on the drugs into their teens.
Psychosocial treatments typically include pharmacological ingestion in addition to rigorous management of behavior in successful treatment of ADHD in children (Daly et al., 1989). Approximately 80% of children undergoing psychiatric therapy for ADHD are prescribed stimulant medication. Recommendations of stimulant medication are common in an effort to reduce hyperactivity and increase performance of tasks such as academic achievement; where a high degree of behavioral control is warranted. Motor skill enhancement in response to methylphenidate is of consistent benefit in the pharmacotherapy tests and in reported performance in the external environment (Wade, 1976). Direct contingency management strategies both at home and in the classroom are typically employed within therapies targeting behavior with modification techniques. As Daly et al. (1989) report, strength of evidence for combined interventions overrules limitations of multi-modality models of treatment, and may even include alternative treatments for comprehensive behavioral management.
Research in this area is extensive, with replication of controlled trials. Correlations linking normative chemical ingestion and ADHD lead to consistent evidence, but with only recent solutions (Schab et al., 2004). In short, food allergy largely “remains an enigma” (Gross et al., 1987). Without consideration of mitigating factors affecting the results of global diet such as stressors, over thirty years of research in the area of hyperkinesis has resulted in little conclusive data. Nevertheless, parental interest in dietary and other alternative options in therapy to pharmaceutical prescription have impacted medical application and scholarship in Complimentary Alternative Medicine (CAM).
According to the American Academy of Pediatrics (AAP), CAM therapies, while popular amongst patients, present a range of challenges in terms of assimilation into the mainstream medical field. The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (NIH) defines CAM as “a group of diverse medical and health care systems, practices, and products that are not presently considered to be part of conventional Western medicine” (Kemper, et al., 2008, p. 1374). This includes widely accepted environmental and integrative therapies such as: 1) Biologically based practices – vitamins, herbs and dietary supplements; 2) Manipulative body based practices – chiropractic, osteopathy, massage therapy, reflexology, Rolfing, Bowen technique and traeger approach; 3) Mind-Body medicine – relaxation, visual imagery and yoga; 4) Bio-field therapies – acupressure, homeopathy, polarity therapy, magnet therapy, Japanese Reiki and Johrei, Chinese qi gong and spiritual healing; and 5) Acupuncture. In addition, the AAP classifies whole or traditional medical systems (i.e. Ayurvedic medicine) in its definition. Pediatric recommendation of CAM therapies to families is supported by AAP Committee Guidelines for Physicians, Counseling Families Who Choose Complementary and Alternative Medicine for their Child with Chronic Illness or Disability.
Licensure restrictions are pertinent to low incidence of recommendation; despite increasing interest by patients. With over one third of adults in the United States reporting participation in such therapies, the disjuncture is discussed as predominantly one of professional consideration rather than patient care. A near absence of formal evaluation and necessary evidence to support CAM recommendation is not present in replicable outcomes. In some cases reports of risk of safety further declination of proposed inculcation of alternative medicine protocol into traditional scientific medicine.
Training in CAM therapies not obligatory, and uneven knowledge of the range of therapies and potential benefits as supplementary modalities to traditional medical intervention, prompts discretionary application rather than a universal buy in. Legal concerns are cited, with information on claims responsive to tortfeasor medical malpractice in this area superseding average pediatric indemnity claims by 37.1%. At present, most CAM therapies outside of chiropractic services are not subject to regulatory oversight. Finally, ethical challenges to CAM by opponents in the AAP articulate concerns over policy adherence, and in particular in regard to unknown, situation specific variables which might contradict oath of practice: 1) respect for patients’ autonomy; 2) nonmaleficence; 3) beneficence; and 4) justice. Recommendation of CAM therapies outside of the United States in Australia and the UK is discussed from the perspective of general practitioners with parallel response (Pirotta, et al. 2000). Limited funding for trials is noted as the main rationale for limited allocation of medical recommendation to CAM therapy resources.
Preliminary research on the relevancy of CAM therapies within the medical field has been conducted by the Medical Expenditure Panel Survey (MEPS) (Davis & Darden, 2003). The MEPS Survey considered children living at home (i.e. not institutionalized), in a questionnaire asking parents if their children had used alternative CAM therapies in the past year. Based on an AP-1 card, the survey outcomes provide a baseline analysis of Boolean statistics classified under sex, age, race, poverty status, region and urban status, correlated with CAM prevalence. The population based statistical analysis proposes to augment future institutional data, and indicate if nothing else, market demand.
The popularity of CAM therapies amongst families avidly seeking solutions to childhood Hyperkinesis and other conditions potentially linked to placebo related disorders, is present a highly accessible, relatively inexpensive and organic approach to combating behavioral imbalances linked to sugar and nervous outbursts (Lim, 2003). A Canadian study conducted by Sinha and Efron (2005) offers some of the most comprehensive data. Incorporation of diet, doctor’s treatment, medication and social factors into the extensive questionnaire with results analyzed in statistical intervals toward dissemination in incremental ratio according to < / > percentage who had tried the therapy, and < / > percentage who found the therapy helpful. The 2003 results revealed up to 51% of children attending outpatient clinics in Victoria had used CAM during the year.
Artificial food colors and other food additives (AFCA) have long been suggested to affect behavior in children, and tested against placebo effect drugs, and sometimes food assimilation (Rose, 1978; and Swanson & Kinsbourne, 1980). The 1975 landmark study on food additives and Hyperkinesis by Dr. Benjamin Fiengold of The Fiengold Association investigated the hypothesis in a double blind test that looked at the removal of food substances for approximate placebo effect in a control group of children: one ingesting additives, and one without (Wender, 1977). The diet excludes petroleum-based preservatives BHT, BHA, TBHQ, synthetic (petroleum-based) dyes and flavorings, and salicylates-containing products. The list of exclusion includes several temperate-zone fruits. The lists of vegetables excluded are peppers, tomatoes and cucumbers. A list other additives, like MSG or sulfites, are also to be avoided. Parents were advised to regularly monitor the diet by maintain a daily diet diary with behavioral notes when beginning the diet (Feingold Assoc, 1998). Observation of psychological impacts from the additive free diet resulted in measurable distance between the additive and additive free groups. In a parallel, yet uncontrolled, version of the study, little behavioral difference was the result. Teachers involved in the study, reported that noted outbursts only occurred after ingestion of bars with food dye, and may have been accompanied by stimulant medication, or even the result of one diet infraction that might lead to global deterioration.
Since the 1975 Fiengold study, numerous replications of the preeminent experiment have been carried out with almost identical accountability (Barling & Bullen, 1980, Kaplan et al, 1989, and Pelsser et al. 2009). Intensification of sugar intake within the studies has led to repeated findings correlating low or high sugar imbalance with Hyperkensis, hypoglycemia and cognitive and behavioral malfunctioning within the subjects. Medical and clinical psychologists have incorporated innovation of possible treatment modalities within the research design, for one or more of ADHD symptoms (Stine, 1976). Nutritional treatment recommended in the prior studies, is an integral approach to regulatory control of the symptoms resultant from body reactions to certain food substances deficiencies (Schnol et al., 2003).
However, previous research studies on the viability of nutritional modalities in the treatment of ADHD indicate several shortcomings that cast doubt on its effectiveness. The research by Schnol et al. (2003) was based on a literature review of studies on the effectiveness of diet regulation to treat ADHD. All studies indicated that diet does not affect ADHD related behaviors among children. Studied variable such as deficiency of fatty acids, sugar levels and food additives did not influence have significant impact in symptoms such as inability to maintain attention, aggressiveness and academic performances. These negative findings, notwithstanding several shortcomings in the methodologies, used highlight the ineffectiveness of nutritional treatment. The sampling procedures were based on information by parents about the perceived abnormal behaviors by their children. It was limited in that parents may not possess sufficient medical knowledge on the nature of ADHD. Their observations could not provide reliable information, since they were not informed by any clinical knowledge of the condition. It is possible that parents regarded it an abnormality or disorder when their children behaved against expectations or in unusual ways. In early childhood, it is not possible to accurately predict the behavior of children. Aggressiveness, for instance, is a common feature of children before the age of seven. Since they lack efficient conversational skills to express themselves through dialogue, they often react emotionally and through physical aggression. When a child breaks objects in anger, it does not necessarily suggest a disorder related to aggressiveness. Therefore, these studies failed to consider the circumstances within which children exhibited ADHD related features. Some studies were carried out in a confined environment such as a laboratory, and this confinement alone, rather than food intake could have affected the children’s behavior. Nonetheless, diet was not found to influence child behavior in a study that place children within a natural setting such as a school environment.
The second limitation is the age of the children in relation to their cognitive development. In his theory of Cognitive Development, Jean Piaget (1969) explains that children’s cognitive skills develop up to the age of seven. In this regard, it is not possible to link their academic performance to nutritional deficiencies. Similarly, aggressiveness is part of child development that has no bearing on diet. Factors such as sugar levels and food additives were found to have effects within five hours, and therefore could not explain a long term condition such as ADHD. Additionally, of the 3 000 food additives and chemicals suggested by Feingold to be associated with the condition, only less than 30 have been studied. This limits the credibility of research findings that links diet regulation to the treatment of ADHD.
Sugar intake has been linked to aggressiveness and hyperactivity in children. A study on the dietary correlates of hyperactive behavior in children was conducted by Prinz, Roberts & Hantman (1980). Primarily, it focused on the influence of sugar intake on child hyperactivity. 28 hyperactive children of ages 4 to 7 were placed on diet regulation, and results analyzed after seven days. In their literature review, they point do previous studies that pointed at ingested substances such as toxins such as lead (David, 1976) and food additives (Williams & Cram, 1958). The authors noted that since food coloring had been associated with hyperactivity, it was possible that other neglected aspects of children’s diet could also have a bearing on their behavior. They pointed out sucrose as one nutritional element that constitute a significant percentage of children’s diet, referring to findings of a survey by the UR Agricultural Research Service in 1965, which found that children aged between six and eleven on average consumed 49 g of sugar daily (Prinz, Roberts &Hantman 1980, p. 762).
The sampling procedure was reliable since most of the children were referred by teachers and psychologists and parents interviewed to rule out cases that did not qualify as a hyperactive condition. Observations were extended to the past two years both at home, in day care centers and school, in terms of being excessively active, moody, restless and slow in completing tasks. They were also screened for any psychological disorder that could have a similar impact n their behavior such as psychosis, mental retardation and neurological impairment. At the same time, children had to exhibit negative effects associated with hyperactivity such as poor academic performance, social interactions and destructive aggressiveness. Another control group of 28 non-ADHD children were picked from the same social setting. The two groups were subjected to the same diet that included sugary products such as candy, dessert and other snacks as well as beverages on the one hand, and foods free of sugar such as refined carbohydrates on the other. Records of their behavior were taken via a video camera in a play room. Variables relevant to the study measured included aggressiveness (tendency to throw or damage objects) and restlessness (repeated movements of arms, fingers, legs and the head). These records were taken for seven days.
However, despite these precautionary efforts to confirm claims of dietary impact on behavior, the findings did not support Feingold’s suggestions since hyperactive behavior was not linked to dietary variables (Prinz, Roberts & Hantman 1980, p. 766). But on the contrary, they cast doubt on the effectiveness of diet regulation such as sugar intake in treating hyperactivity symptoms in children. Nonetheless, agitation was observed to correlate with high sugar intake among the hyperactive group, but not in the control group (Prinz, Roberts & Hantman 1980, p 767).
Comparatively speaking, the 85 % of the sugar products used in this study were impermissible in the Feingold study’s diet, and did not influence behavior in any particular way among the control group. The outcome suggests that nutritional modalities could not reverse hyperactivity and aggression in children. Similarly, high intake of sucrose did not aggravate hyperactivity on ADHD children, an indication that a dietary regulation does not have a significant bearing on the condition. It should also be noted that large amounts of sugars containing sucrose are consumed in carbohydrates in varying amounts by hyperactive and normal children. This scenario makes it difficult to determine the exact levels of sugar intake that could either trigger hyperactivity in non-ADHD children or aggravate it in hyperactive children. As the authors concluded, it is not possible “To discern direction of causality between sugar consumption and hyperactive behaviors, without an experimental manipulation of sugar intake” (Prinz, Roberts & Hantman1980, p. 768). In any case, it should be a long term evaluation to notice significant changes in both the control and sample groups. The variation of sugar intake in either group should lead to significant observable changes in terms of cognitive abilities and hyperactive behaviors for it to be identified as an ADHD treatment factor.
It is also suspected that sugar intake could lead to behavioral changes different from ADHD in normal children. Another observation by the researchers is that diet affects children in different ways, just like stimulants. Therefore, it is not accurate to generalize sugar intake to all cases of ADHD. This perspective is supported in the findings of a research study by Kaplan (1988) which linked hyperactivity to only 8 cases out of 51 children (24 ADHD and 27 in the control group). Lack of significant differences in academic performance indicates that there is no direct relationship between diet and cognitive abilities.
Gross et al. (1987) punched another hole into the Feingold diet in a study on the effects of diets rich in and free from additives on the behavior of children with hyperkinetic and learning disorders. 39 ADHD children from a private school for children with learning disabilities were observed while in a summer camp. all of the children, 17 of which were under medication were subjected to the Feingold diet (free from food additives) for one week, after which the diet was reversed for another week. The sampling procedures had followed recommendations by school psychologists who had noted average to severe cognitive disorders and hyperactivity among the children. Their behavioral tendencies were observed through a videotape at intervals of four minutes. The recorded behaviors were then analyzed in terms of disorganized behavior, misbehavior and motor restlessness. At the end of the study, no correlation was established between diet and behavior among the children, including those under medication. These findings suggested that the Feingold diet did not make any significant positive contribution to the treatment of children with learning disorders hyperactive children under medication (Gross et al.1987, p. 54).
The observations in during the second week in which two children were sent home for indiscipline is hardly related to the ingestion substances forbidden by the Feingold diet. This could be explained in several non-dietary ways. First, the children had consistently complained of the colorless food served in the first week, which they found repulsive. In this light, it is possible that by that the two had rebelled against a restrict diet to which they were not used. It is noted that most had written home in the first week to complain and ask for food supplements. Thus, their behavior was not as a result of the effects of food additives, but possibly a reaction to diet restrictions. Secondly, one of the children was under medication, but was taking an under dose of the prescribed drugs.
Misbehaviors observed were, then, due to lack of proper medication and not a wrong diet. In any case, there are no suggestions that the children were under the Feingold diet prior to the summer camp. Conclusively, nutrition did not have any behavioral impact on ADHD children; either in terms of hyperactivity or learning. Dissemination of the findings from the research correctly indicate that “there seems to be no advantage to the Feingold diet for children with learning disabilities, as far as behavior goes, nor for hyperkinetic children who have responded well to medication” (Gross et al, 1987, p. 55). It then follows that nutritional therapies should not be adapted into the treatment of ADHD in children at the expense of prescribed medication, as it neither treats nor boosts prescribed medicine in treating related symptoms.
In a 1988 study, weakened the nutritional view on childhood hyperactivity was revealed effects of sugar intake among 24 ADHD and 27 non-ADHD preschool boys for three weeks (Kaplan et al., 1988). At the end of the study, no relationship was established between the rate of sugar intake and ADHD symptoms. Only a five out of the 24 ADHD and 3 of the non-ADHD children reflected a correlation, which is hardly a significant phenomenological evidence regarding the treatment of the condition on a nutritional modality. Similar to subsequent findings in the literature (Schnoll et al., 2003) the sampling of the study was restricted to boys exclusively. Limitations to gender control within the study’s sample, is that assumptive bias in gender skews objective findings. Hyperactivity could potentially be explained in terms of Y chromosone genes rather than food substances such sucrose contained in sugar. Similarly, both studies were co-relational, and therefore did not consider the cause effect relationship between sugar intake and hyperactivity. Children who were subjected to the control of a hyperactivity triggering diet did not become aggressive at the end of the study, and neither did the ADHD patients who were fed the recommended diet for treatment show any significant improvement.
The findings were furthered in a study on preschool hyperactive and normal children based its findings on the overall average of daily sugar intake within two weeks. The analysis method used, the Nutrients Assessment System, assessed only mono- and disaccharides such as glucose, sucrose, lactose and fructose. This approach is not comprehensive since other sugar forms like traces of polysaccharides contained in starchy foods could also have an impact on children’s hyperactivity. These sugar forms are contained in most carbohydrates taken by both groups of children.
Outcomes to the study do not clearly indicate how deficiency or over-intake of sugars influences child behavior in one way or the other. The results were negative in studies on protein, calories, carbohydrates and sugar intake. Equally insignificant were studies on the effects of mineral substances such as zinc, manganese, phosphorous, fluoride, calcium and iron. A third study on the preschool children that focused on the essential amino acids did not show any positive relationship between ADHD and food nutrients. Similarly non-significant were results of study on vitamins A, D, C, riboflavin, thiamin, B6 and B12 as well as pantothenic acid.
Researchers conclude that “nutrition behavior interactions are more likely a function of idiosyncratic sensitivities, rather than a general tendency for ADHD children to eat differently from non-ADHD children” (Kaplan et al 127). This was despite the fact that they analyzed results in the final 14 days of the study, an improvement of earlier studies that limited observations to within 7 days. Regardless, they confirmed previous findings that in no way did diet regulation play any significant role in the treatment of hypersensitivity (p 132).
The questionnaire method used in the Sinha and Efron (2005) study augmented inquiries into the authenticity of nutritional research. Several factors noted in the four month period of observation indicated that nutritional treatment does not have any significant impact if used in isolation. The study also showed a combination of various CAM therapies simultaneously. Of the 50 cases which modified diet, 30 indicated that a shift in dietary complex was helpful. The self-reporting is reflective of the 1980 findings of Prinz et al., which indicate that dietary regulations affect ADHD children differently. Only a 24 percent success rate was reported for the use of mineral/vitamins and dietary supplement each.
External factors such as parental response impact the effectiveness of the nutritional modalities. The majority of the parents who responded reported of using a several therapies at the same time (62 percent). In the study, 25 families had used more than 3 therapies, five of which used up to 15 different therapies. Still, it is difficult to attribute any positive improvement to nutrition treatment.
Thirdly, 64 percent of the respondents indicated that their pediatrician was aware of the CAM therapies they were using. This suggests that the doctors could have adjusted their prescriptions accordingly to compliment with the home therapies. In this respect, the achievement of the reported success was most probably as a result of the diet regulation complimenting the doctor’s prescriptions, but hardly the other way round (the medicine complementing the home therapies). In fact, this assumption is substantiated by the fact that 92 percent of the ADHD children were under stimulant medication during the period of the study. They also used other medications which included the antidepressant clonidine, trimeprazine and risperidone (Sinha and Efron, 2005, p 24). The AAP reports that children using CAM “are more likely to be seeing their pediatrician for an illness, take medication on a regular basis, and have ongoing medical problems” (Kemper, et al. 2008, p. 1375).
Most of the families (69 %) attributed their preference of CAM therapies to the need to avoid or minimize side effects caused by prescribed medicines. At least 67 percent reported hope for a cure of their children’s condition as the motivation to use CAM therapies. These factors are a strong indication that complementary and alternative medicines in general and nutrition in particular are effective ways of treating ADHD.
In terms of recommendation of the home therapies, only 10 cases out of 75 were recommended by a doctor, portraying how insignificantly the therapies are regarded within medical cycles. In any case, the definition of CAM therapies by The National Institute of Health in USA as “[. . . ] a broad domain of healing resources that encompasses all health systems, modalities and practices and their accompanying theories and beliefs, other than those intrinsic to the politically dominant health system of a particular society or culture in a given historical period” suggests that they are not supported by substantiated medical facts or authentic research findings. The limitations of CAM as a standardized set of modalities for treatment is not recognized in conventional medicine are outlined in this review.
One of the Sinha and Efron (2005) study’s shortcomings was lack of a control group to authenticate reports on the success of the dietary regulation therapies. A control group of non-ADHD children could have verified whether certain food substances have any impact on the condition. Secondly, the researchers did not specify the nutritional components that were used by parents who adopted the modified diet and mineral/vitamin supplements. Therefore, it is not ascertained whether they are part of Feingold’s diet requirements. The study also did not identify specific aspects of ADHD that were treated by the adopted nutritional therapies. Fourth, the age group of ADHD patients (between 11 and 17 years) was far above the developmental stage at which ADHD is prevalent. This suggests a possibility that behavior could be influenced by psychological factors rather than diet. At this point in the developmental process, individual character traits have formed, and could not be influenced by food substances, with the exception of allergies. Even then, hardly do allergies influence aggression or hyperactivity. And lastly, the findings are based on the reports of parents, in which case adherence to diet specifications is in doubt. Regardless, there was no clear indication that nutrition under CAM therapy influenced child behavior.
Nonetheless, there are outlier studies with evidence showing artificial food colors and additives to cause hyperactivity may hinder learning among normal children. In a study of two groups, 153 three-year old and 144 8-9 year old children, McCann et al. (2007) found that artificial food coloring and additives used as food preservatives had significant effects after they had been ingested. In the study, both groups were given two active mixes and a control placebo. The first mix was concentrated with sodium benzoate than the second one, which was balanced to reflect the participant’s daily intakes in manufactured and processed products. While the typical mix (the second mix) did not have any adverse effects in their behavior, the concentrated mix resulted in significant behavioral changes in terms of hyperactivity and attentiveness. The 3 year old children were affected more, indicating that the effects of food additives and colors diminished gradually with age. They concluded that “the findings, in combination with the replicated evidence for the AFCA effects on the behavior of 3-year-old children, lend strong support for the case that food additives exacerbate hyperactive behaviors (inattention, impulsivity, and over activity) in children at least up to middle childhood” (McCann et al., 2007, p 7).
Experiment did not have a control group to confirm whether the food additives have a serious effect on ADHD children. In linking food additives to hyperactivity, the research findings did not explain whether Feingold’s diet has any positive impact in the treatment of ADHD symptoms. Another factor in the experiment is the use of higher concentrates of sodium benzoate than normally used as a food preservative. It is possible that the chemical could trigger physiological reactions similar to behavior manifestations in children with Attention Deficit and Hyperactivity Disorder. Similarly, the administration of the drinks on a daily basis and subsequent accumulation of chemical sediments in the body could disturb hormonal imbalances in the body and lead to abnormal behaviors, which are not necessarily related to the condition under study. In any case, the findings do not provide a medical explanation on the effectiveness of nutritional therapies in treating ADHD. All it indicates, perhaps, are possible precautionary measures in affected children to avoid aggravating the symptoms.
The prevalence of CAM therapies is quite low, indicating that the treatment modalities either have not been scientifically proved to be effective in treating ADH related symptoms, or they have been found out to be unsuccessful. In the US, a 1996 study of 6262 children aged below 18 by the Medical Expenditure Panel Survey estimated CAM prevalence to be only 2 percent in the total population. Through a statistical analysis of socio-economic and other relevant demographic characteristics, the study found out that the use of complementary and alternative medicine among children was far lower than previously assumed (Davies & Darden, 2003, p. 395). Similarly, it was common in children over 15 years of age. These statistical findings limit the effectiveness of CAM therapies in the treatment of behavior disorders exhibited in ADHD. This is because its use among adolescents and teenage youths could not reverse behaviors that have been established since childhood. On the other hand, nutritional treatment is just a tiny fraction of the 2 percent CAM users. This is a strong pointer to its insignificance in its health value to suffering children. Its ineffectiveness is not limited to unpopularity per se, but partly to the implications reflected by its marginalized use. The authors conclude that CAM therapies such as nutrition treatment have not been standardized so as to provide reliable health care and service procedures.
Other previous studies that linked food additives and colors to behavior disorders were conducted in restricted environments. The research study in 1980 by Swanson and Kinsbourne reported mild and dramatic aversive behaviors. Of the twenty two participants, only two exhibited symptoms that in normal situations could have indicated ADHD related conditions. However, the findings are limited by the fact that the authors noted aversive rather than aggressive behavior that is associated with hyperactivity. In fact, aversive behaviors are manifested in restricted areas where the child’s freedom of expression is limited. Similarly, the child who showed the recorded dramatic behavior change is a three year old girl, and it is not totally uncommon for young children to avoid people.
Terry Rose (1974) had obtained positive findings by studying two children who were hyperactive and previously under the Feingold diet. Upon subjection to a diet consisting of food colors, recorded observations indicated two aspects related to hyperactive disorder. The children exhibited a higher duration of aggressiveness and reduced concentration. Nonetheless, like most other studies, no causal direction was established to determine whether diet regulation improved an ADHD child. In these experiments, what was clearly demonstrated was the aggravation effects of forbidden food substance, rather that the treatment qualities of a modified diet. The research studies have repeatedly failed to show how specific disorder symptoms would be treated if a certain Feingold’s diet was followed. Even more recent studies have not been able to isolate specific symptoms that are either caused or aggravated by food additives. Schab & Trihn (2004, p 423) note that “although neurobehavioral toxicity may characterize a variety of widely distributed chemicals, Improvement in the identification of responders is required before strong clinical recommendations can be made.” This suggests that claims on the effects of food substances eliminated by the Feingold diet and the health value of nutritional therapies in ADHD children are rather generalized. Consequently, psychologists, pediatricians and other medical practitioners have not been able to design specific CAM modalities for specific ADHD symptoms.
It has been more than thirty years since Feingold reported a 50% rate of improvement in behavior among ADHD children in response to placebo like nutrition intake. In spite of the numerous replications of the model study “the Feingold diet is not effective for ADHD, although it may be useful for a small group of children with true sensitivities to food additives” (Chan, 2002, p. 41). The prospectus of the thesis reflects Chan’s assertion; most claims of treatment of ADHD symptoms by nutritional therapies were largely anecdotal, limited to single cases.
If contemporary pediatric medicine today has moved toward alternative therapies, as we have seen throughout the preceding literature review on ADHD, it is largely based on popular demand for holistic therapies, rather than on researched scientific review. Indeed, most patients in treatment chose a modified diet do so “not so much as a result of being dissatisfied with conventional medicine, but largely because they found these health care alternatives to be more congruent with their own values, beliefs, and philosophical orientations toward health and life” (Kemper et al., 2008, p. 1375). The ‘lifestyle’ choice aspect of medical decision making, while not expounded upon throughout the Chapter, nevertheless supports the assertion that diet regulation in particular, and CAM therapy in general do not, on their own, treat Attention Deficit and Hyperactivity Disorder. As Kemper, et al. (2008) maintain, the only assurance given is the guarantee that they are “reasonably expected to be safe.” But equally reasonable is the conclusion that nutritional therapies are expected to be ineffective as far as ADHD is concerned.
Barling, J., and Bullen, G. (2001). Dietary factors and hyperactivity: A failure to replicate. The Journal of Genetic Psychology, 146(1), 177-7. Retrieved from: http://www.heldref.org/pubs/gnt/manuscripts.html
Chan, E., (2002). The role of complementary and alternative medicine in attention-deficit hyperactivity disorder. Developmental and behavioral Pediatrics. 23(1s), s37-45. Retrived from: http://journals.lww.com/jrnldbp/pages/default.aspx
Conners, K. C., Goyette, H. C., Southwick, D. A., Lees, J. M., Andrulonis, P. A. (1976). Food additives and hyperkinesis: A controlled double-blind experiment. The Journal of the American Academy of Pediatrics, 58(2), 154-166. Retrieved from: http://pediatrics.aappublications.org/
Daly, B. P., Creed, T., Xanthopoulos, M., and Brown, R. T. (2007). Psychosocial treatment for children with attention deficit disorder/hyperactivity disorder. Neuropsychology Review, 17(1), 73-89. doi: 10.1007/s11065-006-9018-2
Gross, M. D., Tofanelli, R. A., Butzirus, S. M., Snodgrass, E. W. (1987). The effect of diet rich in and free from additives on the behavior of children with hyperkinetic and learning disorders. The American Academy of Child and Adolescent Psychiatry, 26(1), 53-5. Retrieved from: http://www.aacap.org/
Kaplan, j. B., McNicol, J., Conte, A. R., and Moghadam, H. K. (1989). Overall nutrient intake of preschool hyperactive and normal boys. The Journal of Abnormal Child psychology, 17(2), 127-132. doi: 10.1007/BF00913788.
Kemper, K. J., Vohra, S., and Walls, R. (2008). The use of complementary and alternative medicine in pediatrics. The journal of the American Academy of Pediatrics, 122(6), 1374-1386. doi: 10.1542/peds.2008-2173.
Prinz, R. J., Roberts, W. A., Hantman, E. (1980). Dietary correlates of hyperactive behavior in children. The Journal of Consulting and Clinical Psychology, 48(6), 760-769. Retrived from: http://www.apa.org/pubs/journals/ccp/index.aspx
National Institute of National health (NIH). Retrieved March 5, 2010, from http://www.nimh.nih.gov/health/topics/attention-deficit-hyperactivity-disorder-adhd/index.shtml
Pelesser, L. M. J., Frankena, K., Toorman, J., Savelkoul, H. F. J., Pereira, R. R., and Buitelaar, J. K. (2008). A randomized controlled trial into the effects of food on ADHD. Early child adolescent psychiatry, 18 (1), 12-19. doi: 10.1007/s00787-008-0695-7.
Piaget, J., (1969). Studies in Cognitive Development. Oxford: Oxford University Press.
Rose, T. L., The functional relationship between artificial food colors and hyperactivity (1978). The Journal of Applied Behavior Analysis, 115(4) 439-446. Retrieved from: http://seab.envmed.rochester.edu/jaba/
Schnoll, R., Burshteyn, D., and Cea-Aravena, J. (2003). Nutrition in the treatment of attention-deficit hyperactivity disorder: A neglected but important aspect. Applied Psychophysiology and Biofeedback, 28(1), 63-75. doi: 10.1023/A: 102232101746.
Sinha, D., Efron, D. (2005). Complementary and alternative medicine use in children with attention deficit hyperactivity disorder. Journal of Pediatrics and Child Health, 41(1-2), 23-26. Retrieved from: http://www.wiley.com/bw/journal.asp?ref=1034-4810
Schab, D. W., Trinh, T. Nhi-ha, (2004). Do artificial food colors promote hyperactivity in children with hyperactive syndromes? A metha-analysis of double-blind placebo-controlled trials. Developmental and Behavioral Pediatrics, 25(6), 0196-206X/00/2506-0423. Retrieved from: http://journals.lww.com/jrnldbp/pages/currenttoc.aspx
Stine, J. J. (1976). Symptoms alleviation in the hyperactive child by dietary modification: A report of two cases. American Journal of Othopsychiatry, 46(4), 637-45. Retrieved from: http://www.wiley.com/bw/journal.asp?ref=0002-9432
South, M., and Lim, A. Use of complementary and alternative medicine in children: too important to ignore (2003). The Journal Pediatric Child Health, 39(8), 573-574. Retrieved from: http://www.wiley.com/bw/journal.asp?ref=1034-4810
Swanson, J. M., and Kinsbourne, M. (1980). Food dyes impair performance of hyperactive children on a laboratory learning test. American Association for the Advancement of Science. 207(4438). 1485-1487. Retrieved from: http://www.aaas.org/
Wade, M.G. Effects of methylphenidate on motor skill acquisition of hyperactive children (1976). The Journal of learning Disabilities, 9(7), 443-447. doi: 10.1177/002221947600900711.
Wender, E. H. Food additives and hyperkinesis (1977). The Journal of Diseases children, 131(11), 1204-1206. Retrieved from: http://adc.bmj.com/
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