ADHD Treatments

 
         
 

for Generation Rescue
by Teresa Binstock
June 2008

ADHD Treatments

 

Introduction: Generation Rescue's purpose with these webpages is to provide an overview of research related to ADHD. Medical advice is not given, that's a role reserved for health care providers. Cite 1 & 3 of this ADHD-Treatments section present an overview of mainstream and alternative approaches. Cite 2 is available free online and - along with several others herein - is mainstream in its presentation.


1. Treatment options: summary by Mehl-Madrona, M.D., Ph.D.
Go to: http://www.healing-arts.org/children/
There, link to ADHD, then link to Treatments

2. Managing ADHD in children, adolescents, and adults with comorbid anxiety in primary care
[No authors listed]
Prim Care Companion J Clin Psychiatry. 2007;9(2):129-38.
http://www.psychiatrist.com/pcc/pccpdf/v09n02/v09n0207.pdf
PMID: 17607335


3. Attention deficit/hyperactivity disorder (ADHD) in children: rationale for its integrative management

Kidd PM.
Altern Med Rev. 2000 Oct;5(5):402-28.
http://www.thorne.com/media/attention_deficit.pdf

Attention Deficit/Hyperactivity Disorder (ADHD) is the most common behavioral disorder in children. ADHD is characterized by attention deficit, impulsivity, and sometimes overactivity ("hyperactivity"). The diagnosis is empirical, with no objective confirmation available to date from laboratory measures. ADHD begins in childhood and often persists into adulthood. The exact etiology is unknown; genetics plays a role, but major etiologic contributors also include adverse responses to food additives, intolerances to foods, sensitivities to environmental chemicals, molds, and fungi, and exposures to neurodevelopmental toxins such as heavy metals and organohalide pollutants. Thyroid hypofunction may be a common denominator linking toxic insults with ADHD symptomatologies. Abnormalities in the frontostriatal brain circuitry and possible hypofunctioning of dopaminergic pathways are apparent in ADHD, and are consistent with the benefits obtained in some instances by the use of methylphenidate (Ritalin) and other potent psychostimulants. Mounting controversy over the widespread use of methylphenidate and possible life-threatening effects from its long-term use make it imperative that alternative modalities be implemented for ADHD management. Nutrient deficiencies are common in ADHD; supplementation with minerals, the B vitamins (added in singly), omega-3 and omega-6 essential fatty acids, flavonoids, and the essential phospholipid phosphatidylserine (PS) can ameliorate ADHD symptoms. When individually managed with supplementation, dietary modification, detoxification, correction of intestinal dysbiosis, and other features of a wholistic/integrative program of management, the ADHD subject can lead a normal and productive life.
PMID: 11056411


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4. Attention patterns in children with attention deficit disorder with or without hyperactivity

Zalsman G et al.
ScientificWorldJournal. 2003 Nov 13;3:1093-107.

The objective of this study was to differentiate the attention patterns associated with attention deficit disorder with or without hyperactivity using continuous performance test (CPT). The diagnoses were based on the DSM-III, III-R, and IV criteria and of the 39 children who participated in the study, 14 had attention deficit disorder with hyperactivity (ADDH) and 11 had attention deficit disorder without hyperactivity (ADDWO), while 14 normal children served as a control group. Attention patterns were examined according to the performance of subjects on the CPT and parental scores on the ADHD Rating Scale, the Child Attention Profile, and the Conners Rating Scale. CPT performances were assessed before and after administration of 10 mg methylphenidate. We found as hypothesized that the CPT differentiated between the ADDH and ADDWO groups. However, contrary to our expectations, the ADDH children made more omission errors than the ADDWO children; they also showed more hyperactivity and impulsivity. The performance of both groups improved to an equal degree after the administration of methylphenidate. It is concluded that different subtypes of the attention deficit disorders are characterized by different attention profiles and that methylphenidate improves scores on test of continuous performance.
PMID: 14625396


5. Attention-deficit/hyperactivity disorder: etiology and pharmacotherapy

Noorbala AA, Akhondzadeh S.
Arch Iran Med. 2006 Oct;9(4):374-80.

Attention-deficit/hyperactivity disorder is a common neurobehavioral disorder of childhood and adolescence. The etiology of attention-deficit/hyperactivity disorder is not well understood. Neurochemical studies suggest, alterations in catecholaminergic, mainly dopaminergic and noradrenergic, transmitter functions markedly contribute to the symptoms of this disorder. The symptoms of attention-deficit/hyperactivity disorder are significantly ameliorated by the agents that specifically influence these neurotransmitters. Animal studies implicate areas of the brain in which these neurotransmitters are most dominant. Psychostimulant medications are generally the first choice in the treatment of attention-deficit/hyperactivity disorder. Approximately 70% of the children treated show improvement in the primary attention-deficit/hyperactivity disorder symptoms and in comorbidity such as conduct disorder, although the benefits may not hold beyond two years. Despite the well-established efficacy and safety of stimulants for attention-deficit/hyperactivity disorder, alternative medicines are still needed for several reasons. About 30% of children and adolescents with this disorder may not respond to stimulants or may be unable to tolerate potential adverse events such as decreased appetite, mood lability and sleep disturbances. Although stimulants do not increase the risk for later substance abuse in attention-deficit/hyperactivity disorder, concerns have been raised about special prescription rules and a potential for abuse by persons other than the attention-deficit/hyperactivity disorder subjects. This review focuses on etiology, assessment, and treatment of attention-deficit/hyperactivity disorder.
PMID: 17061613


6. Dopamine transporter genotype influences the physiological response to medication in ADHD

Gilbert DL et al.
Brain. 2006 Aug;129(Pt 8):2038-46.
http://brain.oxfordjournals.org/cgi/content/full/129/8/2038

Attention deficit hyperactivity disorder (ADHD) is a complex, multifactorial disorder characterized by physical hyperactivity and behavioural disinhibition. Short interval cortical inhibition (SICI), measured in motor cortex with transcranial magnetic stimulation, is reduced in ADHD and correlates with symptom severity. However, ADHD medication-induced changes in SICI vary widely among normal individuals and have not been well studied in children with ADHD. Therefore, we undertook this study to measure and compare effects of two ADHD medications, methylphenidate (MPH), a psychostimulant, and atomoxetine (ATX), a selective norepinephrine reuptake inhibitor, on SICI in children with ADHD. In addition, we wished to determine whether a genetic variation in the dopamine transporter (DAT1), a site of action of MPH, could influence the effects of MPH or ATX on SICI. We performed a randomized, double-blind, single-dose, crossover study comparing 0.5 mg/kg MPH with 1.0 mg/kg ATX in 16 children with ADHD, aged 8-17. Seven were homozygotes and 9 heterozygotes for the DAT1 variable number of tandem repeats 10-repeat allele. Medication and genotype effects on SICI were estimated with repeated measures, mixed model regression. We found that MPH and ATX had similar effects on SICI. However, medication effects differed significantly by DAT1 genotype [F(2,13) = 13.04, P = 0.0008]. Both MPH and ATX increased SICI in heterozygotes but not in 10-repeat homozygotes. In conclusion, MPH and ATX have similar effects on SICI in children with ADHD. A genetic variation in DAT1, previously linked to ADHD risk and MPH behavioural responses, influences the neurophysiological effects of both MPH and ATX.
PMID: 16760197


7. Olive oil and mitochondrial oxidative stress

Mataix J, Ochoa JJ, Quiles JL.
Int J Vitam Nutr Res. 2006 Jul;76(4):178-83.

This review summarizes studies on the role of olive oil intake in the prevention and attenuation of mitochondrial oxidative stress derived from several situations such as ageing, physical exercise, treatment with adriamycin or intake of thermally oxidised oils. After more than fifteen years of studies on these issues, results have demonstrated that under different models of oxidative stress the regular intake of virgin olive oil as dietary fat is able to attenuate or increase free radical production at the mitochondrial level to a lower extent than when n-6 polyunsaturated oils are used. In the same way, virgin olive oil leads to better function of the mitochondrial electron transport chain.
PMID: 17243080


8. Diet, genetic polymorphisms, detoxification, and health risks

Lampe JW.
Altern Ther Health Med. 2007 Mar-Apr;13(2):S108-11.

Modulation of detoxification enzymes is one mechanism by which diet may influence risk of cancer and other diseases. However, genetic differences in taste preference, food tolerance, nutrient absorption, and metabolism and response of target tissues all potentially influence the effect of diet on disease risk. Thus, disease prevention at the individual and population level needs to be evaluated in the context of the totality of genetic background and exposures to both causative agents and chemopreventive compounds. Polymorphisms in the detoxification enzymes that alter protein expression and/or function can modify risk in individuals exposed to the relevant substrates. Diet is a mixture of carcinogens, mutagens, and protective agents that are all metabolized by detoxification enzymes. Genotypes associated with more favorable handling of carcinogens may be associated with less favorable handling of phytochemicals. For example, glutathione S-transferases (GST) detoxify polycyclic aromatic hydrocarbons present in grilled meats. GSTs also conjugate isothiocyanates, the chemopreventive compounds found in cruciferous vegetables. Polymorphisms in the GSTM1 and GSTT1 genes result in complete lack of GSTM1-1 and GSTT1-1 proteins, respectively. In some observational studies of cancer, cruciferous vegetable intake confers greater protection in individuals with these polymorphisms; however, in other studies, the converse is observed. A recent study of sulforaphane pharmacokinetics suggests that lack of the GSTM1 enzyme is associated with more rapid excretion of sulforaphane. Many phytochemicals are also conjugated with glucuronide and sulfate moieties, and are excreted in urine and bile. Polymorphisms in UDP-glucuronosyltransferases (UGT) and sulfotransferases (SULT) may contribute to the variability in phytochemical clearance and efficacy. The effects of UGT polymorphisms on flavonoid clearance have not been examined, but UGT polymorphisms affect glucuronidation of several drugs and steroid hormones. Genetic polymorphisms in detoxification enzymes may account in part for individual variation in disease risk but have to be considered in the context of other aspects of human genetics, gut bacterial genetics, and environmental exposures.
PMID: 17405687

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