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Hitam-Putih Autis Di Indonesia

June 9, 2008
June 9, 2008

Assalamualaikum… Saya bukan ahli. CMIIW saya hanya sedih melihat pemberitaan yang tidak berimbang. Tulisan ini saya kumpulkan dari berbagia sumber. Siapa tahu bermanfaat….. —————————————————————————————————————- Pada hari Selasa, 6 Mei 2008, Koran Tempo menurunkan berita berjudul Menurunkan Resiko Autisme (http://www.korantempo.com/korantempo/2008/05/06/Gaya_Hidup/krn,20080506,69.id.html) Quote : Dampak merkuri pada janin akan terkonsentrasi dalam plasenta selama masa kehamilan. Konsentrasi dalam janin delapan kali lipat, terutama dalam hati, ginjal, dan otak. Jika sang ibu terkontaminasi pada waktu menyusui, merkuri dapat mengalir melalui air susu ibu dan diabsorpsi dengan baik oleh bayi. Untuk itu, sangat penting seorang wanita mempersiapkan kehamilan. MARLINA Langkah Persiapan Ibu Hamil 1.Keluarkan semua tambalan amalgam dari gigi. 2.Beri tenggang waktu tiga bulan sebelum hamil untuk mengeluarkan toksin tubuh. 3.Bila kadar merkuri tinggi pada ibu, lakukan dulu detoksifikasi sebelum hamil. 4.Jangan makan ikan laut selama hamil dan menyusui. dst…. Pada Sabtu, 7 Juni 2008, Koran Kompas memuat berita berjudul “Boom” Autisme Terus Meningkat (http://cetak.kompas.com/read/xml/2008/06/07/01452123/boom.autisme.terus.meningkat) Quote : “Jika ibu menyatakan kalau setelah divaksinasi, kondisi si anak kemudian makin mundur, kita cari apakah anak ini keracunan merkuri. Darahnya harus diperiksa untuk mencari tahu berapa kadar logam berat, logam merkuri, diperiksa rambutnya, apakah merkurinya sudah lama menumpuk di tubuh dan tidak bisa keluar, misalnya, papar Melly Budhiman.” …. “Faktor pemicu autisme itu banyak, tidak mungkin satu pemicu saja. Selain keracunan logam berat, anak-anak penyandang autisme biasanya juga mengalami alergi, kondisi pencernaannya juga jelek, kata Melly. Ada kecurigaan, salah satu faktor pencetus autisme adalah logam berat merkuri.” …. “Repotnya, menurut Melly, banyak vaksin yang beredar di pasaran mengandung merkuri. Satu suntikan vaksin dari luar negeri biasanya merkuri yang dikandung 25 mikrogram. Bahkan, ada vaksin yang kandungan merkurinya lebih dari itu. Keterkaitan vaksin sebagai pencetus autisme masih jadi perdebatan di dunia internasional. Ini tentunya perlu penelitian lebih lanjut,ujarnya” —————————————————————————————— Masyarakat awam seperti saya semakin binggung…apalagi yang ngomong mempunyai sederet gelar. Siapa yang mesti diikuti…??? Senjata saya hanya satu…tanya Paman Google….namun..sekali lagi namun…..saya ingatkan…hati-hati dalam mencari informasi….carilah sumber yang benar-benar reliable…biasanya situs-situs resmi pemerintah….karena pemberitaan seputar autis di internet lebih banyak yang pseudoscince. Sebenarnya siapa dr. Melly Budiman ini…. Mohon maaf…tanpa bermaksud mendeskriditkan beliau….beliau ini aktif di DAN (Defeat Autism Now) yang dengan gencarnya melakukan publikasi di media-media baik lokal maupun internasional. DAN!(Defeat Autism Now!) ini adalah organisasi yang terdiri dari peneliti dan juga ilmuwan yang terbentuk tahun 1995 dibawah lindungan ARI(Autism Research Institue) yaitu sekumpulan orang tua yang anaknya menderita autisme. Didirikan tahun 1967 oleh Dr. Bernard Rimland di US, adalah seorang psikolog dimana anaknya yang bernama Mark Rimland menyandng autis berat. Lembaga ini adalah lembaga yang berkecimpung dalam terapi alternative untuk autism dan neurodevelopmental disorder lainnya. Jelas bentuk terapi dan pemikirannya bukanlah ilmu kedokteran. Namun karena menggunakan berbagai istilah medik dan mengatakan berbagai ilmunya juga riset, maka masyarakat akhirnya terkelabuhi juga. Bentuk ilmu ini adalah PSEUDOSCIENCE karena berbagai yang diaku sebagai risetnya itu tidak memenuhi standard procedure penelitian ilmiah kedokteran. Siapa saja dokter Indonesia yang masuk dalam daftar DAN : Melly Budhiman, M.D. Jalan Beton No. 9 (77) Jakarta 13210 Indonesia ph: 62-21-4892332 fax: same Rudy Sutadi, Dr. SpA, M.D. JL Buncit Raya No. 15 Jakarta Selatan 12740 Indonesia ph: 62-79-408-36/7 fax: 62-21-794-0838 Kurniati Ihromi Tanjung, M.D. Ave. Alfredo Jahn con Tercera Transv. Qta. Emaus. Urb Los Chorros Caracas 1071 Indonesia ph: (58) 212-2371051 fax: (58) 212-2387339 Sasanti Yuntar, M.D. Ketintang Selatan 8/14 Surabaya 60232 Indonesia ph: 62-31-8380114 Sumber : http://www.autismwebsite.com/ari-lists/danforeign.html DAN! 2003 FALLCONFERENCE Sunday October 5: General Session JAQUELYN McCANDLESS, M.D. INTERVENTIONS for Digestive, Immune, and Neurological Problems in Autism Spectrum Disorder INTERVENTIONS • AFTER HISTORY, EXAMINATION, AND LABORATORY TESTING: • TREATMENT CATEGORIES: • • 1) DIET, NUTRITION, NUTRIENTS, FOOD ALLERGY • 2) GUT HEALTH, TREATING INFLAMMATION, PATHOGENS • 3) TOXIC ACCUMULATION, VARIOUS DETOXIFICATION – CHELATION METHODS • 4) IMMUNE ISSUES, VIRAL OVERLOAD • 5) PSYCHOTROPICS: SSRI’S, STIMULANTS, ANTI-PSYCHOTICS, ANTI-CONVULSANTS DIAGNOSTIC EVALUATION LAB WORKUP GENERAL • • Routine Laboratory Screening (Any good lab will do these – insurance almost always pays) • • 1) CBC w Differential and Platelets • 2) Chemistry Panel Including Liver Enzymes • 3) Thyroid Panel • 4) Urinalysis • 5) Plasma zinc, serum copper, ceruloplasmin SPECIALTY LABORATORY TESTS • • General Biochemical (Must order kits from Specialty Labs – Insurance variably pays for these tests) • • 1) Amino Acids (Plasma) • 2) Organic Acid (Urine) • 3) Comprehensive Stool Analysis • 4) IgG 90-Food Delayed Sensitivity (Plasma) • 5) Fatty Acids (Plasma) • 6) Vitamin levels (Plasma) • 7) Hair Analysis, RBC Minerals • 8) Immune Tests Incl. Metallothionein BIOCHEMICAL IMBALANCES IN ASD CHILDREN • Multiple nutritional deficiencies • Elevated IgG antibodies to milk and wheat • Imbalance of gut bacterial flora • Elevated urinary bacterial metabolites • Evidence of myelin sheath injury in brain • Evidence of immune impairment NUTRIENT DEFICIENCIES • B6 and Magnesium • Zinc, Selenium and other minerals • Calcium • Vitamins A, C, & E • Essential Fatty Acids • Amino Acids • B-Vitamins: B1, 2, 3, 5, 12, & Folate GUT I – CLINICAL HISTORY: EARLY INDICATIONS OF GUT DYSFUNCTION 1) Familial digestive dysfunctions 2) Inability to breast feed 3) Persistent colic in infancy 4) Frequent infections (e.g. ear) leading to frequent antibiotics 5) Reaction to certain immunizations GUT II – GASTROINTESTINAL PATHOLOGY SYMPTOMS REPORTED BY PARENTS • • Persistent diarrhea and/or constipation, bloating, gas, abdominal pain • Self-restriction of diet • Night waking • Greater allergic susceptibilities GUT III: G.I. HEALTH: Treatments That Parents Can Do • •Eliminate sugars and junk food for everyone in the family Read labels on foods, get educated about toxins in both food and water • GF/CF/SF, SCD Diet • Enzymes and Probiotics • Basic Nutrient Supplementation GUT IV: G.I. HEALING: Treatments That Require a Doctor’s Prescription • Lab Testing Must be Practitioner-Ordered • Anti-Fungal Prescription Treatment • Anti-Bacterial (Clostridia and other) Prescription Treatment • Secretin, Vit. B12 shots, IV Glutathione • Immunoglobulin, IV or Oral Summary: TREATMENT FOR GUT DISORDER AND NUTRIENT DEFICIENCIES • • GF/CF/SF or SCD, Other Special Diets • Removal of other offending foods per tests • Replace nutrient deficiencies • Treat for pathogen overgrowth; probiotics, if seriously infested, systemic anti-fungals. If mild, natural antidotes, e.g. Lauricidin, Grapefruit Seed Extract, Aqua Flora TOXINS DIAGNOSTIC EVALUATION 1) Heavy Metals Exposure, History 2) Hair Elements Evaluation DD 3) RBC Minerals 4) Metallothionein, plasma zinc, serum copper, ceruloplasmin 5) Gut readiness, OAT to r/o pathogens 6) Mineralization readiness, vits/mins especially zinc seterusnya bisa baca di: http://64.202.182.52/powerpoint/dan2003/JacquelineMcCandless_files/frame.htm ————————————————————————————————- Yuk kita coba telusuri sedikit demi sedikit…terkait dengan pemberitaan Koran Tempo dan Kompas terkait statment yang dibuat dr. Melly Budiman. 1.Keluarkan semua tambalan amalgam dari gigi. berikut jawaban dari ADA (American Dental Association) ADA Positions & Statements ADA Statement on Dental Amalgam Revised: April 2007 Dental amalgam (silver filling) is considered a safe, affordable and durable material that has been used to restore the teeth of more than 100 million Americans. It contains a mixture of metals such as silver, copper and tin, in addition to mercury, which binds these components into a hard, stable and safe substance. Dental amalgam has been studied and reviewed extensively, and has established a record of safety and effectiveness. Issued in late 1997, the FDI World Dental Federation and the World Health Organization consensus statement on dental amalgami stated, “No controlled studies have been published demonstrating systemic adverse effects from amalgam restorations.” The document also states that, aside from rare instances of local side effects of allergic reactions, “the small amount of mercury released from amalgam restorations, especially during placement and removal, has not been shown to cause any . adverse health effects.” The ADA’s Council on Scientific Affairs’ 1998ii report on its review of the recent scientific literature on amalgam states: “The Council concludes that, based on available scientific information, amalgam continues to be a safe and effective restorative material.” The Council’s report also states, “There currently appears to be no justification for discontinuing the use of dental amalgam.” In an articleiii published in the February 1999 issue of the Journal of the American Dental Association, researchers report finding “no significant association of Alzheimer’s Disease with the number, surface area or history of having dental amalgam restorations” and “no statistically significant differences in brain mercury levels between subjects with Alzheimer’s Disease and control subjects.” In 2002, the U.S.Food and Drug Administration (FDA) and other organizations of the U.S. Public Health Service (USPHS) that continue to investigate the safety of dental amalgams released a consumer update stating that there is “no valid scientific evidence has shown that amalgams cause harm to patients with dental restorations, except in the rare case of allergy.” A 2003 paper published in the New England Journal of Medicineiv states, “Patients who have questions about the potential relation between mercury and degenerative diseases can be assured that the available evidence shows no connection.” In 2004, an expert panel reviewed the peer-reviewed, scientific literature published from 1996 to December 2003 on potential adverse human health effects caused by dental amalgam and published a report. The review was conducted by the Life Sciences Research Office (LSRO) and funded by the National Institutes of Dental and Craniofacial Research, National Institutes of Health and the Centers for Devices and Radiological Health, U.S.Food and Drug Administration (FDA). The resulting report states that, “The current data are insufficient to support an association between mercury release from dental amalgam and the various complaints that have been attributed to this restoration material. These complaints are broad and nonspecific compared to the well-defined set of effects that have been documented for occupational and accidental elemental mercury exposures. Individuals with dental amalgam-attributed complaints had neither elevated urinary mercury nor increased prevalence of hypersensitivity to dental amalgam or mercury when compared with controls.” The full report is available from LSRO (www.lsro.org). A summary of the review is published in Toxicological Reviewsv. In 2006, the Journal of the American Medical Association (JAMA) and Environmental Health Perspectives published the results of two independent clinical trials designed to examine the effects of mercury release from amalgam on the central and peripheral nervous systems and kidney function. The authors concluded that “there were no statistically significant differences in adverse neuropsychological or renal effects observed over the 5-year period in children whose caries are restored using dental amalgam or composite materials”;vi,vii and “children who received dental restorative treatment with amalgam did not, on average, have statistically significant differences in neurobehavioral assessments or in nerve conduction velocity when compared with children who received resin composite materials without amalgam. These finding, combined with the trend of higher treatment need later among those receiving composite, suggest that amalgam should remain a viable dental restorative option for children.”viii The ADA supports ongoing research in the development of new materials. However, the ADA continues to believe that amalgam is a valuable, viable and safe choice for dental patients. Footnotes i.FDI Policy Statement/WHO Consensus Statement on Dental Amalgam . September 1997. (accessed March 8, 2007) ii. ADA Council on Scientific Affairs. Dental Amalgam: Update on Safety Concerns. J Am Dent Assoc. 1998;129:494-503. iii. Saxe SR et al. Alzheimer’s disease, dental amalgam and mercury. J Am Dent Assoc. 1999;130:191-9. iv. Clarkson TW, Magos L, Myers GJ. The toxicology of mercury – Current exposures and clinical manifestations. N Engl J Med. 2003;349:1731-7. v. Brownawell AM et al. The Potential Adverse Health Effects of Dental Amalgam. Toxicol Rev. 2005;24:1-10. vi. Bellinger DC, Trachtenberg F, Barregard L, Tavares M, Cernichiari E, Daniel D, McKinlay S. Neuropsychological and Renal Effects of Dental Amalgam in Children: A Randomized Clinical Trial. JAMA 2006;295:1775-83. vii. Bellinger DC, Daniel D, Trachtenberg F, Tavares M, KcKinlay. Dental Amalgam Restorations and Children’s Neuropsychological Function: The New England Children’s Amalgam Trial. Environ Health Perspect (online 30 October 2006). viii. DeRouen TA, Martin MD, Leroux BG, Townes BD, Woods JS, Leitao J, Castro-Caldas A, Luis H, Bernardo M, Rosenbaum G, Martins IP. Neurobehavioral Effects of Dental Amalgam in Children: A Randomized Clinical Trial. JAMA 2006;295:1784-92. Return to Top Page Updated: April 06, 2007 http://www.ada.org/prof/resources/positions/statements/amalgam.asp 2. Faktor pemicu autisme itu banyak, tidak mungkin satu pemicu saja. Selain keracunan logam berat, anak-anak penyandang autisme biasanya juga mengalami alergi, kondisi pencernaannya juga jelek, kata Melly. Ada kecurigaan, salah satu faktor pencetus autisme adalah logam berat merkuri. Berikut jawabannya : Separating Fact from Fiction in the Etiology and Treatment of Autism:A Scientific Review of the Evidence James D. Herbert, Ph.D.Ian R. Sharp, Ph.D.Brandon A. Gaudiano, Ph.D. Autistic-spectrum disorders are among the most enigmatic forms of developmental disability. Although the cause of autism is largely unknown, recent advances point to the importance of genetic factors and early environmental insults, and several promising behavioral, educational, and psychopharmacologic interventions have been developed. Nevertheless, several factors render autism especially vulnerable to pseudoscientific theories of etiology and to intervention approaches with grossly exaggerated claims of effectiveness. Despite scientific data to the contrary, popular theories of etiology focus on maternal rejection, candida infections, and childhood vaccinations. Likewise, a variety of popular treatments are promoted as producing dramatic results, despite scientific evidence suggesting that they are of little benefit and in some cases may actually be harmful. Even the most promising treatments for autism rest on an insufficient research base, and are sometimes inappropriately and irresponsibly promoted as “cures.” We argue for the importance of healthy skepticism in considering etiological theories and treatments for autism. Note: We use the term “autism” throughout this paper to refer not only to classic autistic disorder (American Psychiatric Association, 1994), but in some cases to the full range of autistic-spectrum disorders. The vast majority of the research reviewed in this paper does not distinguish among the various subtypes of autistic-spectrum disorders. It is therefore often impossible to judge the degree to which research findings are unique to autistic disorder per se, or are generalizable to other pervasive developmental disorders. This article was first published in the Spring-Summer edition of The Scientific Review of Mental Health Practice. Autism is a pervasive developmental disorder marked by profound deficits in social, language, and cognitive abilities. Prevalence rates range from 7 to 13 cases per 10,000 (Bryson, 1997; Bryson, Clark, & Smith, 1988; Steffenberg & Gillberg, 1986; Sugiyama & Abe, 1989). It is not clear if the actual prevalence of autism is increasing, or if the increased frequency of diagnosis has resulted from wider recognition of the disorder and especially recognition of the full range of pervasive developmental disorders, often referred to as “autistic-spectrum disorders.” Either way, autism is no longer considered rare, occurring more commonly than Downs syndrome, cystic fibrosis, and several childhood cancers (Fombonne, 1998; Gillberg, 1996). The degree of impairment associated with autism varies widely, with approximately 75% of autistic individuals also meeting criteria for mental retardation (American Psychiatric Association [APA], 1994). Autism occurs three to four times more frequently in males than females (Bryson et al., 1988; Steffenberg & Gillberg, 1986; Volkmar, Szatmari, & Sparrow, 1993). Although recent advances have been made with respect to possible causal factors (Rodier, 2000), the exact etiology of autism remains unknown. Moreover, although certain behavioral, educational, and pharmacological interventions have been demonstrated to be helpful for many individuals with autism, there is currently no cure for the disorder. WHY AUTISM IS FERTILE GROUND FOR PSEUDOSCIENCE Several factors render autism especially vulnerable to etiological ideas and intervention approaches that make bold claims, yet are inconsistent with established scientific theories and unsupported by research (Herbert & Sharp, 2001). Despite their absence of grounding in science, such theories and techniques are often passionately promoted by their advocates. The diagnosis of autism is typically made during the preschool years and, quite understandably, is often devastating news for parents and families. Unlike most other physical or mental disabilities that affect a limited sphere of functioning while leaving other areas intact, the effects of autism are pervasive, generally affecting most domains of functioning. Parents are typically highly motivated to attempt any promising treatment, rendering them vulnerable to promising “cures.” The unremarkable physical appearance of autistic children may contribute to the proliferation of pseudoscientific treatments and theories of etiology. Autistic children typically appear entirely normal; in fact, many of these children are strikingly attractive. This is in stark contrast to most conditions associated with mental retardation (e.g., Downs syndrome), which are typically accompanied by facially dysmorphic features or other superficially evident abnormalities. The normal appearance of autistic children may lead parents, caretakers, and teachers to become convinced that there must be a completely “normal” or “intact” child lurking inside the normal exterior. In addition, as discussed above, autism comprises a heterogeneous spectrum of disorders, and the course can vary considerably among individuals. This fact makes it difficult to identify potentially effective treatments for two reasons. First, there is a great deal of variability in response to treatments. A given psychotropic medication, for example, may improve certain symptoms in one individual, while actually exacerbating those same symptoms in another. Second, as with all other developmental problems and psychopathology, persons with autism sometimes show apparently spontaneous developmental gains or symptom improvement in a particular area for unidentified reasons. If any intervention has recently been implemented, such improvement can be erroneously attributed to the treatment, even when the treatment is actually ineffective. In sum, autisms pervasive impact on development and functioning, heterogeneity with respect to course and treatment response, and current lack of curative treatments render the disorder fertile ground for quackery. A number of contemporary treatments for autism can be characterized as pseudoscientific. Most scientists agree that there are no hard- and-fast criteria that distinguish science from pseudoscience; the differences are in degree, rather than kind (Bunge, 1994; Herbert et al., 2000; Lilienfeld, 1998). Although a detailed treatment of pseudoscience in mental health is beyond the scope of this paper, a brief discussion of the features that distinguish it from legitimate science is important in order to provide a context for considering currently popular etiological theories and treatments for autism. In general, pseudoscience is characterized by claims presented as being scientifically verified even though in reality they lack empirical support (Shermer, 1997). Pseudoscientific treatments tend to be associated with exaggerated claims of effectiveness that are well outside the range of established procedures. They are often based on implausible theories that cannot be proven false. They tend to rely on anecdotal evidence and testimonials, rather than controlled studies, for support. When quantitative data are considered, they are considered selectively. That is, confirmatory results are highlighted, whereas unsupportive results are either dismissed or ignored. They tend to be promoted through proprietary publications or Internet Web sites rather than refereed scientific journals. Finally, pseudoscientific treatments are often associated with individuals or organizations with a direct and substantial financial stake in the treatments. The more of these features that characterize a given theory or technique, the more scientifically suspect it becomes. A number of popular etiological theories and treatment approaches to autism are characterized by many of the features of pseudoscience described above (Green, 1996a; Green, 2001; Herbert & Sharp, 2001; Smith, 1996). Still other treatments, although grounded on a sound theoretical basis and supported by some research, are nonetheless subject to exaggerated claims of efficacy. What follows is a review of the most popular dubious theories and questionable intervention approaches for autism. We also review promising etiologic theories and treatments. Some intervention programs are designed specifically for young children, whereas others are applied across a wider age range. THE ETIOLOGY OF AUTISM: SEPARATING FACT FROM FICTION Psychoanalytic Explanations Although modern theories of autism posit the strong influence of biological factors in the etiology of the disorder, psychoanalytic theories have abounded traditionally. Kanner (1946) was the first to describe the parents of children with autism as interpersonally distant. For example, he concluded that the autistic children he observed were “kept neatly in refrigerators which did not defrost” (Kanner, 1973, p. 61). However, Kanner also stressed that the disorder had a considerable biological component that produced disturbances in the formation of normal emotional contact. It was Bruno Bettelheim who was perhaps the most influential theorist promoting psychoanalytic interpretations of autism. Bettelheim rose to prominence as director of the University of Chicagos Orthogenic School for disturbed children from 1944 to 1978. He rejected Kanners conclusions positing a biological role in the etiology in autism and was convinced that autism was caused by “refrigerator” mothers. According to Bettelheim, autistic symptoms are viewed as defensive reactions against cold and detached mothers. These unloving mothers were sometimes assumed to be harboring “murderous impulses” toward their children. For example, in his book The Empty Fortress, Bettelheim (1967) wrote that one autistic girls obsession with the weather could be explained by dissecting the word to form “we/eat/her,” indicating that she was convinced that her mother, and later others, would “devour her.” Based on his conceptualization of autism, Bettelheim promoted a policy of “parentectomy” that entailed separation of children from their parents for extended periods of time (Gardner, 2000). Other psychoanalytic therapists such as Mahler (1968) and Tustin (1981) promoted similar theories positing problems in the mother- child relationship as causing autism (see Rosner, 1996, for a review of psychoanalytic theories of autism). After his suicide in 1990, stories began to emerge that tarnished Bettelheims reputation (Darnton, 1990). Several individuals claimed abuse at the hands of the famous doctor when they were at the Orthogenic School. Furthermore, information emerged that Bettelheim often lied about his background and training. For example, although he frequently claimed to have studied under Freud in Vienna, Bettelheim possessed no formal training in psychoanalysis whatsoever, and instead held a degree in philosophy. Also, Bettelheim claimed that 85% of his patients at the Orthorgenic School were cured after treatment; however, most of the children were not autistic and the case reports he presented in his books were often fabrications (Pollak, 1997). Despite the continued acceptance of Bettelheims theories in some circles, no controlled research has been produced to support the refrigerator mother theory of autism. For example, Allen, DeMeyer, Norton, Pontus, and Yang (1971) did not find differences between parents of autistic and mentally retarded children and matched comparison children on personality measures. Despite the complete absence of controlled evidence, even today some psychoanalytic theorists continue in the tradition of Bettelheim by highlighting the putative role of early mother-child attachment dysfunctions in causing autism (Rosner, 1996). Candida Infection Candida albicans is a yeastlike fungus found naturally in humans that aids in the destruction of dangerous bacteria. Candidiasis is an infection caused by an overgrowth of candida in the body. Women often contract yeast infections during their childbearing years. In addition, antibiotic medication can disrupt the natural balance among microorganisms in the body, resulting in an overgrowth of candida (Adams & Conn, 1997). In the 1980s, anecdotal reports began to emerge suggesting that some children with candidiasis later developed symptoms of autism. Supporters of this theory point to animal studies in which candida was shown to produce toxins that disrupted the immune system, leading to the possibility of brain damage (Rimland, 1988). Furthermore, Rimland speculated that perhaps 5 to 10% of autistic children could show improved functioning if treated for candida infection. Proponents often recommend that Nystatin, a medication used to treat women with yeast infections, be given to children whose mothers had candidiasis during pregnancy, whether or not the children show signs of infection. However, there is no evidence that mothers of autistic children have a higher incidence of candidiasis than mothers in the general population and only uncontrolled case reports are presented as evidence for the etiological role of candida infection in autism (Siegel, 1996). Adams and Conn (1997) presented the case study of a 3-year-old autistic boy who reportedly showed improved functioning following a vitamin treatment for candida infection. However, the boy was never medically diagnosed with candidiasis and was only reported to meet criteria based on questionnaire data. In addition, reports of the childs functioning were mostly based on parental report (especially concerning functioning prior to the course of vitamin treatment) and not on standardized assessment instruments. Although interesting, such presentations provide no probative data on the possible role of candidiasis in causing autism. Without reliable and valid evidence to the contrary, case reports cannot rule out a host of confounding variables, including any natural remission or change in symptoms due to developmental maturation or even merely to the passage of time. It is important to remember that many people, especially women, contract candidia infections at different points in their lives, sometimes without even knowing that they are infected because the symptoms are so mild (Siegel, 1996). However, there is no evidence that even severe candidiasis in humans can produce brain damage that leads to the profound deficits in functioning found in autism. MMR Vaccination There has recently been much public concern that the mumps, measles, and rubella (MMR) vaccine is causing an increased incidence of autism. As evidence of the link between the MMR vaccine and autism, proponents point to the fact that reported cases of autism have increased dramatically over the past two decades, which appear to coincide with the widespread use of the MMR vaccine starting in 1979. In fact, Dales, Hammer, and Smith (2001) found in their analyses of California Department of Developmental Services records that the number of autistic disorder caseloads increased approximately 572% from 1980 to 1994. Indicating a similar trend in Europe, Kaye, Melero-Montes, and Jick (2001) reported that the yearly incidence of children diagnosed with autism increased sevenfold from 1988 to 1999 in the United Kingdom. Fears that the MMR vaccine may be responsible for this rise in the increasing incidence of autism have been picked up in the media and some parents have decided to decline vaccinations for their children in an effort to protect them from developing autism (Manning, 1999). Rimland (2000) saw “medical overexuberance” as producing a tradeoff in which vaccinations protect children against acute diseases while simultaneously increasing their susceptibility to more chronic disorders, including autism, asthma, arthritis, allergies, learning disabilities, Crohns disease, and attention deficit hyperactivity disorder. Pointing out that the average number of vaccines school- age children receive is now at 33, Rimland blamed the “vaccine industry” for making products that have not been properly tested before their widespread usage. He concluded by stating that research on this problem should be of the “highest priority.” In fact, it was preliminary research findings that initially raised the possibility that the MMR vaccine might be related to the apparent increase in the incidence of autism. The British researcher Andrew Wakefield and colleagues (1998) reported 12 case studies of children who were diagnosed with particular forms of intestinal abnormalities (e.g., ileal-lymphoid-nodular hyperplasia). Eight out of the 12 children demonstrated behavioral disorders diagnosed as representing autism, which reportedly occurred after MMR vaccination. The authors concluded that “the uniformity of the intestinal pathological changes and the fact that previous studies have found intestinal dysfunction in children with autistic-spectrum disorders, suggests that the connection is real and reflects a unique disease process” (p. 639). However, Wakefield et al. made it clear in their report that they did not prove an actual causal connection between the MMR vaccine and autism. Although the Wakefield et al. (1998) case reports suggested that the MMR vaccine may be associated with autism, recent epidemiological research has provided strong evidence against any such connection. Kaye et al. (2001) conducted a time trend analysis on data taken from the UK general practice research database. As discussed earlier, they found that the yearly incidence of diagnosed autism increased dramatically over the last decade (0.3 per 10,000 persons in 1988 to 2.1 per 10,000 persons in 1999). However, the prevalence of MMR vaccination among children remained virtually constant during the analyzed time period (97% of the sample). If the MMR vaccine were the major cause of the increased reported incidence of autism, then the risk of being diagnosed with autism would be expected to stop rising shortly after the vaccine was instated at its current usage. However, this was clearly not the case in the Kaye study, and therefore no time correlation existed between MMR vaccination and the incidence of autism in each birth order cohort from 1998 to 1993. In an analogue study in the United States, Dales et al. (2001) found the same results when using California Department of Developmental Services autism caseload data from the period 1980 to 1994. Once again, the time trend analysis did not show a significant correlation between MMR vaccine usage and the number of autism cases. Although MMR vaccine usage remained fairly constant over the observed period, there was a steady increase of autism caseloads over the time studied. It is important to note that the increased incidence of autism found in these two studies most likely reflects an increased awareness of autism-spectrum disorders by professionals and the public in general, along with changes in diagnostic criteria, rather than a true increase in the incidence of the disorder (Kaye et al., 2001). Most recently, the U.S. governments Institute of Medicine, in a comprehensive report cosponsored by the National Institutes of Health and the Centers for Disease Control and Prevention, recently concluded that there exists no good evidence linking the MMR vaccine and autism (Stratton, Gable, Shetty, & McCormick, 2001). The MMR hypothesis reveals several important lessons for the student of autism. First, parents and professionals alike can easily misinterpret events that co-occur temporally as being causally related. The fact that the MMR vaccine is routinely given at around the same age that autism is first diagnosed reinforces the appearance of a link between the two. Second, the MMR-autism link reveals nicely the self-correcting nature of science. Like many hypotheses in science, the MMR-autism hypothesis, although reasonable when initially proposed, turned out to be incorrect or at best incomplete. Third, the issue illustrates the persistence of incorrect ideas concerning the etiology and treatment of autism even in the face of convincing evidence to the contrary. For example, Rimland (2000) purported to warn the public of the dangers of child vaccinations because of their link to autism and begins his article with the decree: “First, do no harm.” However, recent research indicates that the MMR vaccine cannot be responsible for the sharp increases in diagnosed autism, and the real harm is the public health concern raised by encouraging parents to avoid vaccinating their children from serious diseases that can easily be prevented. Current Scientific Findings Research has implicated genetic factors, in utero insults, brain abnormalities, neurochemical imbalances, and immunological dysfunctions as contributing to autism. Siblings of individuals with autism have about a 3% chance of having the disorder, which is 50 times greater than the risk in the general population. In monozygotic twins, if one twin has autism, the second has a 36% chance of being diagnosed with the disorder and an 82% chance of developing some autistic symptoms (Trottier, Srivastava, & Walker, 1999). Although not definitive, the higher concordance rates in monozygotic twins relative to fraternal siblings suggests a genetic contribution to the etiology of autism. Nevertheless, the lack of 100% concordance for monozygotic twins suggests that the disorder probably develops as the result of combined effects of genetic and environmental factors. Genetic disorders that have been identified as producing an increased risk of developing autism or pervasive developmental disorders include tuberous sclerosis, phenylketonuria, neurofibromatosis, fragile X syndrome, and Rett syndrome (Folstein, 1999; Trottier et al., 1999). Recent findings have also implicated a variation of the gene labeled HOXA1 on chromosome 7 as doubling the risk of autism, although this is only one of the many possible genes linked to the disorder (Rodier, 2000). Nevertheless, although some gene variants may increase the risk of developing autism, other variants may act to decrease the risk, explaining the large variability in the expression of autism. Rubella infection of the mother during pregnancy and birth defects resulting from ethanol, valproic acid, and thalidomide exposure are also known in utero risk factors (Rodier, 2000). However, these factors can only explain the development of autism in a small subset of individuals. Regarding time for increased vulnerability, evidence from individuals exposed to thalidomide now points to the conclusion that the in utero insults that increase the risk of the autism probably occur quite early, within the first trimester of gestation (Stromland, Nordin, Miller, Akerstrom, & Gillberg, 1994). Other research that has compared individuals with autism with those without the disorder found differences in brain wave activity, brain (e.g., cerebellar) structures, and neurotransmitter levels (Trottier et al., 1999). Scientific evidence supports the conclusion that autism is a behavioral manifestation of various brain abnormalities that likely develop as the result of a combination of genetic predispositions and early environmental (probably in utero) insults. Although recent scientific discoveries provide important clues to the development of the disorder, the etiology of autism is complex and the specific causes are still largely unknown. Summary of Etiologic Theories and Research There is currently no empirical support for theories that implicate unloving mothers, yeast infections, or childhood vaccinations as the cause of autism. The evidence invoked in support of these claims involves uncontrolled case studies and anecdotal reports. The confusion about the causes of autism appears to stem largely from illusory temporal correlations between the diagnosis of the disorder and normal events occurring in early childhood. No research has demonstrated a differential risk for autism due to maternal personality characteristics, the presence of candidiasis, or the use of the MMR vaccine. Scientific evidence points to genetic predispositions and various early environmental insults to the developing fetus as responsible for the development of the disorder. QUESTIONABLE TREATMENTS FOR AUTISM: BOLD CLAIMS, DUBIOUS THEORIES, AND LITTLE DATA A number of interventions have been promoted as providing breakthroughs in the treatment of autism. These treatments share many of the features of pseudoscience described earlier. Despite the absence of supportive data and even in the face of contradictory data, these treatments continue to be passionately promoted by their supporters. Sensory-Motor Therapies Smith (1996) reported that over 1,800 variations of sensory-motor therapy have been developed to treat individuals with autism. The popularity of these approaches derives from the observation that many individuals with autism exhibit sensory-processing abnormalities, although these types of dysfunctions are neither universal nor specific to the condition (Dawson & Watling, 2000). Furthermore, many individuals with autism exhibit a relatively high prevalence of fine and gross motor impairments. Nevertheless, little controlled research has examined the effectiveness of sensory-motor treatments for autism. We next briefly review the most commonly promoted treatments for autism that emphasize the importance of ameliorating the sensory-motor deficits often associated with the disorder. Facilitated Communication Facilitated communication (FC) is a method designed to assist individuals with autism and related disabilities to communicate through the use of a typewriter, keyboard, or similar device.PROMISING TREATMENTS FOR AUTISM: REVIEWING THE EVIDENCE AND REINING IN CLAIMS The interventions reviewed thus far give little reason for hope in the treatment of autism. Fortunately, the situation is not so bleak. Several promising programs have been developed. Although some research has been conducted on these programs, none has been sufficiently evaluated using experimental research designs. In effect, no treatment currently meets the criteria established by the American Psychological Associations Committee on Science and Practice as an empirically supported treatment for autism (Gresham, Beebe-Frankenberger, & MacMillan, 1999; Rogers, 1998). Nevertheless, the intervention programs reviewed in the following section are based on sound theories, are supported by at least some controlled research, and clearly warrant further investigation. Applied Behavior Analysis Among the currently most popular interventions for autism are programs based on applied behavior analysis (ABA), an approach to behavior modification rooted in the experimental analysis of behavior, in which operant conditioning and other learning principles are used to change problematic behavior (Cooper, Heron & Heward, 1989). Several intervention programs for autism based on ABA methods have been developed. Rogers (1998) noted that many studies of behavioral interventions for autism have focused on a single discrete symptom, and that such interventions have often been shown to be quite effective for such limited targets. In contrast to the single-symptom approach, some programs have been designed to target the core deficits of autism and thereby improve the overall functioning of autistic individuals. By far the most popular of these programs are modeled after the Young Autism Project (YAP) developed at the University of California at Los Angeles by O. Ivar Lovaas and colleagues. Initiated in 1970, the YAP aims to improve the functioning of young children with autism through the use of an intensive, highly structured behavioral program delivered one-on-one by specially trained personnel. The program is designed to be implemented full-time during most of the childs waking hours, and family involvement is deemed to be critical. Treatment is initially delivered in the clients home, with eventual progression to community and school settings. The program is often referred to as “discrete trial training,” reflecting the fact that each specific intervention utilizes a discrete stimulus-response-consequence sequence. For example, a child might be presented with three blocks of different colors, and given the verbal stimulus “touch red.” If the child touches the red block, a reward is provided (e.g., a small snack, verbal praise). Lovaas (1981) described the program in a treatment manual designed for parents and professionals. The YAP was evaluated in a widely cited study by Lovaas (1987), with long-term follow-up data reported by McEachlin, Smith, and Lovaas (1993). Lovaas (1987) treated 19 young children with the ABA program described above for 40 or more hours per week for at least 2 years. Two control conditions were employed, one in which 19 children received 10 hours or less per week of the ABA program (minimal treatment condition), and another in which 21 children received unspecified community interventions but no ABA. Outcome measures were IQ and educational placement. Lovaas (1987) reported dramatic results: After at least 2 years of intervention, almost half (47%) of the experimental group was found to have IQ scores in the normal range, and were reported to be functioning in typical first grade classrooms without special support services. Lovaas described these children as having “recovered” from autism. Only one child from either of the two control groups demonstrated similar gains. In addition, there were large differences in IQ scores between the experimental group and the two control groups. McEachlin et al. (1993) followed up participants from the experimental and minimal ABA treatment conditions several years later. The difference in IQ scores between the two groups was maintained. Of the 9 children with the best outcomes from the original report, 8 continued to function in regular education classrooms. Not surprisingly, a great deal of enthusiasm was generated by these reports, and demand for ABA programs modeled after the YAP has grown rapidly since their publication. Unlike other treatment or educational programs, the YAP offered not only the possibility of significant improvement in functioning, but also suggested that a substantial number of autistic youngsters could achieve completely normal functioning. Several commentators, however, raised serious concerns about the conclusions reached by Lovaas (1987) and McEachlin et al. (1993). Schopler, Short, and Mesibov (1989) noted that the outcome measures employed, IQ and school placement, might not reflect true overall functional changes. Increases in IQ scores, for example, could reflect increased compliance with testing rather than true changes in intellectual abilities, and school mainstreaming may be more a function of parental and therapist advocacy and changing school policies than increased educational functioning per se. In addition, Schopler et al. argued that the participants in the YAP study appeared to be relatively high- functioning individuals with good prognosis, and were unrepresentative of the larger population of autistic children. Most importantly, they pointed out that the study design was not a true experiment, as subjects were not randomly assigned to the experimental and control groups. They suggested that the procedures for assigning subjects to groups likely resulted in important differences between the experimental and control conditions that may have contributed to the observed outcome differences. Schopler et al. (1989) concluded that that “it is not possible to determine the effects of this intervention” from this study (p. 164). Others subsequently raised similar criticisms. Gresham and MacMillan (1997, 1998) expanded on the threats to both internal and external validity raised by Schopler et al. (1989) and called for “healthy skepticism” in evaluating the claims of the YAP studies. Mesibov (1993) expressed concerns about pretreatment differences between the experimental and control groups, and about the many domains of functioning in which deficits commonly associated with autism (e.g., social interactions and conceptual abilities) that were not assessed. Mundy (1993) raised similar concerns, noting that many high-functioning autistic individuals achieve IQ levels in the normal range, thereby raising questions about the use of IQ scores to measure “recovery” from autism. Although they uniformly take exception with the claims of “recovery” from autism proffered by Lovaas and colleagues, even these critics concede that the YAP study yielded promising results that merit further investigation. Although several studies of similar ABA interventions have now been published, two points about these studies are noteworthy. First, each is methodologically even weaker than the original YAP study. Second, the results of these studies, although generally promising, fall significantly short of those obtained by Lovaas (1987) and McEachlin et al. (1993). Birnbrauer and Leach (1993) reported on 9 children who received 19 hours per week of a one-on-one ABA program for 2 years, and 5 control children who received no ABA. Four of the 9 children in the experimental group made significant gains in IQ, relative to 1 of the 5 control children, although none of the participants achieved completely normal functioning. Sheinkopf and Siegel (1998) conducted a retrospective study of 11 children who received between 12 and 43 hours per week of home-based ABA programs for between 7 and 24 months, relative to a matched control group of children who received unspecified school-based treatment. Data were obtained through record reviews of an existing database. Relative to the control group, children in the experimental group achieved higher gains in IQ, although few differences emerged between the groups in autistic symptoms. Finally, in an uncontrolled, pre-post design study, Anderson, Avery, DiPietro, Edwards, and Christian (1987) reported on 14 children who received between 15 and 25 hours per week of home- based ABA for 1 year. Modest gains were reported in mental age scores and communication skills for most children, although those with the lowest baseline functioning made essentially no progress. In addition, no children were able to be integrated into regular educational settings. All of these studies involved ABA programs modeled on Lovaass YAP, in which services were delivered one-on-one in the childs home, although each study differed from the original YAP study in several respects (e.g., the number of hours per week of intervention, the duration of the program, the nature and training of the therapists). Two additional studies evaluated similar ABA interventions, in which services were delivered in school- or center-based programs. Fenske, Zalenski, Krantz, and McClannahan (1985) compared 9 children who began receiving an ABA program through the Princeton Child Development Institute prior to the age of 60 months, relative to 9 who enrolled after the age of 60 months. After at least 2 years of treatment, 4 of the 9 children in the younger group were enrolled in regular school classes, relative to 1 of the 9 children from the older group. No data were provided on autistic symptoms or functioning level. Harris and colleagues reported pre-post data on children treated with an ABA program through the Douglas Developmental Center of Rutgers University. Harris, Handleman, Gordon, Kristoff, and Fuentes (1991) reported average IQ gains of approximately 19 points after 10 to 11 months of intervention. It should be noted that this sample of children was relatively high functioning, with an average pretreatment IQ of 67.5 and with symptoms rated as “mild to moderate.” Nevertheless, despite the observed gains in IQ, all children were described as having significant impairments after treatment. Taken together, the literature on ABA programs for autism clearly suggest that such interventions are promising. Methodological weaknesses of the existing studies, however, severely limit the conclusions that can be drawn about their efficacy. Of particular note is the fact that no study to date has utilized a true experimental design, in which subjects were randomly assigned to treatment conditions. This fact limits the inferences that can be drawn about the effects of the programs studied. Moreover, these concerns are compounded by pretreatment differences between experimental and control conditions in each of the studies reviewed. Other methodological concerns include questions about the representativeness of the samples of autistic children, unknown fidelity to treatment procedures, limited outcome data for most studies, and problems inherent in relying on IQ scores and school placement as primary measures of autistic symptoms and functioning. S o what are we to make of the claims that ABA programs, and those modeled after the YAP in particular, can result in “recovery” from autism? After more than 30 years since its initiation and 14 years since the first published outcome report, no study has replicated the results of the original YAP study and several critics have challenged its conclusions. Subsequent research has yielded more modest gains in functioning, casting further doubt on the claims that autistic youngsters can be “cured” through ABA programs. Nevertheless, these caveats have not tempered the enthusiasm of some proponents of ABA programs. Consider, for example, the following quotes from leading advocates of ABA intervention programs for autism: Several studies have now shown that one treatment approachtearly, intensive instruction using the methods of Applied Behavior Analysistcan result in dramatic improvements for children with autism: successful integration in regular schools for many, completely normal functioning for some. . . . No other treatment for autism offers comparable evidence of effectiveness. (Green, 1996b, p. 29; emphasis in original) There is little doubt that early intervention based on the principles and practices of Applied Behavior Analysis can produce large, comprehensive, lasting, and meaningful improvements in many important domains for a large proportion of children with autism. For some, those improvements can amount to achievement of completely normal intellectual, social, academic, communicative, and adaptive functioning. (Green, 1996b, p. 38) Furthermore, we also now know that applying effective interventions when children are very young (e.g., under the age of 3c4 years) has the potential for achieving substantial and widespread gains and even normal functioning in a certain number of these youngsters. (Schreibman, 2000, p. 374) During the past 15 years research has begun to demonstrate that significant proportions of children with autism or PDD who participate in early intensive intervention based on the principles of applied behavior analysis (ABA) achieve normal or near-normal functioning. . . . (Jacobson, Mulick, & Green, 1998, p. 204) It is difficult to justify such assertions in light of the extant scientific literature on ABA programs for autism. Ironically, many of these same authors have been highly critical of the exaggerated claims made for nonbehavioral interventions. Clearly, ABA programs do not possess most of the features of pseudoscience that typify many of the highly dubious treatments for autism. ABA programs are based on well-established theories of learning and emphasize the value of scientific methods in evaluating treatment effects. Nevertheless, given the current state of the science, claims of “cure” and “recovery” from autism produced by ABA are misleading and irresponsible. Other Comprehensive Behavioral Programs Although ABA programstthe YAP in particulartare the best-known behavioral interventions for autism, other programs have been developed that draw to varying degrees on behavioral learning principles. One of the most significant ways in which these programs differ from the ABA programs described earlier is that they make no claims of “curing” autism. Rather, they strive to ameliorate the functioning of autistic individuals by utilizing a variety of educational and therapeutic strategies. Few studies have been conducted on these programs, and those that have utilize only pre- post research designs, thereby limiting the conclusions that can be drawn. LEAP Hoyson, Jamieson, and Strain (1984) described the effects of a program known as Learning Experiences: An Alternative Program for Preschoolers and Parents (LEAP). The LEAP program is composed of an integrated preschool and a behavior-management skills training program for parents. The preschool program, which was one of the first to integrate normally developing children with those with autism, blends normal preschool curricula with activities designed specifically for children with autism. Peer modeling is encouraged in an effort to develop play and social skills. The parental skills- training component aims to teach parents effective behavior- management and educational skills in natural contexts (i.e., home and community). In a pre-post study, Hoyson et al. (1984) reported accelerated developmental rates in 6 “autistic-like” children over the course of their participation in the LEAP program. Strain, Kohler, and Goldstein (1996) reported that 24 out of 51 children were attending regular education classes, although no information was provided regarding functioning level or special school supports. Although certain aspects of the LEAP program appear promising, the paucity of the available research, and especially the absence of controlled research, preclude judgments about its usefulness. Denver Health Sciences Program Developed by Sally Rogers and colleagues at the University of Colorado School of Medicine, the Denver Health Sciences Program is a developmentally oriented preschool program designed not only for children with autism-spectrum disorders, but varied other behavioral problems. Several pre-post studies have reported that autistic children participating in the program demonstrated accelerated developmental rates in several domains, including language, play skills, and social interactions with parents (Rogers & DiLalla, 1991; Rogers, Herbison, Lewis, Pantone, & Reis, 1986; Rogers & Lewis, 1989; Rogers, Lewis, & Reis, 1987). Once again, the lack of controlled research makes it impossible to draw firm conclusions about the effectiveness of this program. Project TEACCH The program for the Treatment and Education of Autistic and Related Communication Handicapped Children (TEACCH) is a university-based project founded by Eric Schopler at the University of North Carolina at Chapel Hill (Schopler & Reichler, 1971). TEACCH programs have become among the more widely used intervention programs for autism. Project TEACCH incorporates behavioral principles in treating children with autism, but differs from ABA in several fundamental ways. Most significantly, TEACCH focuses on maximizing the skills of children with autism while drawing on their relative strengths, rather than attempting “recovery” from the disorder. The program is designed around providing structured settings in which children with autism can develop their skills. Teachers establish individual workstations where each child can practice various tasks, for example, such visual-motor activities as sorting objects by color. Visual cues are often provided in an effort to compensate for the deficits in auditory processing often characteristic of autism. Like the YAP, LEAP, and Denver programs, TEACCH emphasizes a collaborative effort between treatment staff and parents. For example, parents are encouraged to establish routines and cues in the home similar to those provided in the classroom environment (Gresham, Beebe-Frankenberger, & MacMillan, 1999). Only two treatment outcome studies to date have investigated the effectiveness of project TEACCH. Schopler, Mesibov, and Baker (1982) collected questionnaire data from 348 families whose children were currently or previously enrolled in the program. Individuals with autism who participated ranged in age from 2 to 26, and ranged cognitively from severe mental retardation to normal intellectual functioning. The majority of respondents indicated that the program was helpful. Also, the institutionalization rate of participants was 7%, as compared with the rates of 39% to 75% reported for individuals with autism in the general population based on data from the 1960s. Nevertheless, this study is marked by many serious methodological weaknesses. These include a highly heterogeneous sample (not all participants had autism), the absence of a meaningful control condition, and the lack of standardized and independent assessment measures. In addition, Schopler and colleagues comparison of the institutionalization rate in their study with 1960s data is probably misleading. Changes in government policy during the 1960s and 1970s led to decreased institutionalization rates in general (Smith, 1996). More recently, Ozonoff and Cathcart (1998) tested the effectiveness of TEACCH home-based instruction for children with autism. Parents were taught interventions for preschool children with autism focusing on the areas of cognitive, academic, and prevocational skills related to school success. The treatment group was composed of 11 preschool children with autism who received 4 months of home programming. The treatment group was assessed before and after treatment with the Psychoeducational ProfilecRevised (Schopler, Reichler, Bashford, Lansing, & Marcus, 1990), and results were compared with those from a matched comparison group of children not in the TEACCH program who were similarly assessed. Results showed that the preschool children receiving TEACCH-based parent instruction improved significantly more in the areas of imitation, fine-motor, gross-motor, and nonverbal conceptual skills. Furthermore, the treatment group showed an average developmental gain of 9.6 months after the 4-month intervention. Although this study provides some support for the TEACCH program, the conclusions are tempered by methodological limitations, including the lack of a randomized control condition and the absence of treatment fidelity ratings. Summary of Behavioral Intervention Programs Several programs utilizing various behavioral and developmental intervention strategies have been shown to yield promising results in the treatment of children with autism. Among the most promising are programs based on the intensive, one-on-one application of applied behavior analysis (ABA). Some proponents of ABA have made sweeping claims about the ability of such programs to “cure” autism that are not supported by the available literature. Other behaviorally based programs (e.g., LEAP, Denver Health Sciences Program, TEACCH) have been less prone to exaggerated claims. However, the available research on these programs is more akin to program evaluations than to traditional studies of treatment efficacy or effectiveness. For example, no studies have employed experimental designs, and none has used objective measures of the full range of symptoms and functional impairments associated with autism. Component analysis studies have not evaluated the specific mechanisms responsible for the programs effects, and no research has compared the relative effectiveness of various behavioral programs. Dawson and Osterling (1997) identified six features that are common to most comprehensive early-intervention programs for autism. They suggested that these “tried-and-true” features, rather than the specific methods emphasized by each program, may be responsible for the observed effects of early-intervention programs. These common features include (a) curriculum content emphasizing selective attention, imitation, language, toy play, and social skills; (b) highly supportive teaching environments with explicit attention to generalization of gains; (c) an emphasis on predictability and routine; (d) a functional approach to problem behaviors; (e) a focus on transition from the preschool classroom to kindergarten, first grade, or other appropriate placements; and (f) parental involvement in treatment. Several of these features were incorporated into the treatment recommendations for autism made by the American Academy of Child and Adolescent Psychiatry (AACAP, 1999). Further research is clearly indicated to assess the effects of each of these components, and to evaluate potential additive effects of the specific elements of various early intervention programs. Pharmacotherapy A detailed review of the psychopharmacologic treatment of autism is beyond the scope of this paper, and several excellent recent reviews are available (AACAP, 1999; Aman & Langworthy, 2000; Campbell, Schopler, Cueva, & Hallin, 1996; Gillberg, 1996; King, 2000). Although not curative, in open-label case reports several medications appeared to improve various symptoms associated with autism, thereby increasing individuals ability to benefit from educational and behavioral interventions. With a few noteworthy exceptions, few studies have utilized double-blind, placebo- controlled designs, especially with autistic children. The most extensively studied agents are the dopamine antagonists, especially haloperidol (Haldol). Several well-controlled studies have shown haloperidol to be superior to placebo for a number of symptoms, including withdrawal, stereotypies, and hyperactivity (Anderson et al., 1984; Campbell et al., 1996; Locascio et al., 1991), although drug-related dyskinesias appear to be relatively common following long-term administration (Campbell et al., 1997). There is growing interest in the atypical neuroleptics, risperidone (Risperdal) in particular. In a double-blind, placebo-controlled trial with autistic adults, McDougle et al. (1998) found risperidone to be superior to placebo on several measures, and to be well tolerated. Several studies suggest the usefulness of various selective serotonin reuptake inhibitors (SSRIs), including fluvoxamine (Luvox; McDougle et al., 1996), fluoxetine (Prozac; Cook et al., 1992; DeLong, Teague, & Kamran, 1998; Fatemi, Realmuto, Khan, & Thuras, 1998), and clomipramine (Anafranil; Gordon et al., 1992; 1993). However, SSRIs are often associated with intolerable adverse events. For example, recent open-label studies reveal significant rates of adverse side effects of clomipramine, including seizures, weight gain, constipation, and sedation (e.g., Brodkin et al, 1997). Moreover, there is a growing consensus that children appear to respond less well to SSRIs than do adolescents and adults (Brasic et al., 1994; McDougle, Kresch, & Posey, 2000; Sanchez et al., 1996). Tricyclic antidepressants are less frequently used relative to SSRIs, given the possibility of cardiovascular side effects and lowering of seizure threshold. Although little research has examined anxiolytic agents in autism, what little research has been conducted suggests that they are of little benefit. In fact, Marrosu et al. (1987) found increases in hyperactivity and aggression following treatment with the benzodiazepine diazepam (Valium). More promising results have been obtained in open-label studies of buspirone (Buspar; McCormick, 1997; Realmuto, August, & Garfinkel, 1989; Ratey, Mikkelsen, & Chmielinski, 1989). THE HARM IN PROMOTING UNPROVEN TREATMENTS As the previous review illustrates, even the most promising treatments for autism are typically far from ideally effective, leaving the autistic individual with substantial impairments. It is therefore natural for parents, educators, and even mental health professionals to ask what the harm is in trying an unproven treatment. This is a difficult question for which there is no easy answer. On the one hand, we are not suggesting that parents and professionals not be allowed to explore a range of treatment options. What we are suggesting is that they do so with as much information as possible, and armed with an attitude of healthy skepticism. For several reasons, such skepticism is particularly important in considering treatments for autism. First, proponents of many treatments, both novel and established, often make impressive claims that are simply not supported by controlled research. Moreover, many mental health and educational professionals who work with autistic individuals have been reluctant to speak out against pseudoscientific theories and practices. This silence places the burden directly on consumers to become educated about the empirical status of various treatment options. Unless they make efforts to become informed about the research literature themselves, consumers can be easily misled and given false hope. Second, no treatment is without cost. Aside from the obvious financial burden, there are always other costs to consider when contemplating a new treatment. In particular, time and resources spent on an unproven therapy are time and resources that could have been spent on an intervention with a greater likelihood of success (what economists term “opportunity cost”). This point is especially critical with respect to early-intervention programs, as a growing literature suggests the importance of early intervention with specialized behavioral and educational programs (Fenske, Zalenski, Krantz, & McClannahan, 1985). The issue of cost is complicated by the tendency, in the absence of appropriate control conditions, to misattribute any positive changes that may be observed to an intervention and then expend even more resources on that intervention when the improvement may not be due to the treatment. Alternatively, repeated experience with treatments that are promoted with much fanfare but turn out to be ineffective might cause family members of autistic individuals to become unnecessarily cynical about even legitimate interventions. Finally and perhaps most importantly, one must always be aware of the potential for harm. There are numerous examples in the history of pharmacotherapy of substances that were initially believed to be therapeutically useful and devoid of harmful side effects that turned out to be quite harmful (e.g., combined fenfluramine and dexfenfluramine, thalidomide). The effects of long-term use of substances like secretin and DMG have not been investigated and are therefore unknown. The risk of harm is not limited to pharmacologic interventions, however. Consider, for example, the case of FC. The cases of family members being convicted of abuse and sent to prison based on alleged communications provides a sobering example of the harm that can arise from unvalidated interventions. Despite the wealth of scientific data demonstrating that the “facilitator” is the source of such messages, some courts still permit communications derived via FC to be used as evidence (Gorman, 1999). 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A., & Schwartz, A. A. (1993). An experimental assessment of facilitated communication. Mental Retardation, 31, 49c59. Whiteley, P., Rodgers, J., Savery, D., & Shattock, P. (1999). A gluten-free diet as an intervention for autism and associated spectrum disorders: Preliminary findings. Autism, 3, 45c65. Zollweg, W., Palm, D., & Vance, V. (1997). The efficacy of auditory integration training: A double blind study. American Journal of Audiology, 6, 39c47. Quackwatch Home Page This article was posted on June 13, 2003. http://www.quackwatch.org/01QuackeryRelatedTopics/autism.html #wwww.medscape.com/viewarticle/463573_print – 6k Evidence does not support thimerosal-autism link – Literature Monitor Clinician Reviews, Oct, 2003 The health care community has been uncertain about whether thimerosal, a mercury based preservative found in some vaccines, is a contributing factor for the seeming increased prevalence of autistic disorder (see Hudson GT, Dixon D. Autism: challenges in diagnosis and treatment [Board Review]. Clinician Reviews. 2003;1317]:45-52). However, the results of a Danish population-based study published in Pediatrics did not show such a correlation. For their analysis, Madsen et al obtained information from a Danish national database regarding 956 children who were diagnosed with autism from age 2 up to (but not including) their 10th birthday between 1971 and 2000. Children who followed a full vaccination schedule between 1961 and 1970 received a total of 400 mg of thimerosal by age 15 months; from 1970 to 1992, children received a total of 250 ug by age 10 months. Thimerosal-containing vaccines were discontinued in Denmark in March 1992. Data showed that autism incidence remained stable until 1990. In 1991, the incidence began to rise, but the greatest increases occurred after the discontinuation of thimerosal. The rate of incidence peaked in 1999; children between the ages of 2 and 6 who were diagnosed with autism that year had been born after the introduction of thimerosal-free vaccines. The spike in the incidence of autism after 1990 may be attributable to increased attention to the disorder, as well as to a change in the diagnostic criteria that occurred in 1994, the authors suggest. Furthermore, they caution that their data “cannot, of course, exclude the possibility that thimerosal at doses larger than [those] used in Denmark may lead to neuro developmental damage.” Madsen KM, Lauritsen MB, Pedersen CB, et al. Thimerosal and the occurance of autism: negative ecological evidence from Danish population-based data. Pediatrics. 2003;12:604-606. COPYRIGHT 2003 Clinicians Publishing Group COPYRIGHT 2003 Gale Group Original article : http://www.mmrthefacts.nhs.uk/news/newsitem.php?id=77 MMR news 10-Sep-04: New research finds no link between MMR and autism Study published in the Lancet show that children who received MMR vaccine were no more likely to develop autism than those who did not. The results of a major new study were published in the Lancet today. The study examined the medical records of nearly 1300 children in the UK diagnosed with autism or similar conditions, and compared them to a control group of over 4,500 children. The results showed that children who received the combined MMR vaccine were no more likely to develop autism than those children who did not receive the jab. The lead research Dr Liam Smeeth said “We hope the results of this study, the most robust and comprehensive undertaken to date, will reassure parents that MMR is not associated with increased risk of developing autism.” The article can be accessed via the Lancet website http://www.thelancet.com/journal Original article : http://www.mmrthefacts.nhs.uk/news/newsitem.php?id=76 MMR news 15-May-04: No evidence for links between autism, MMR and measles virus Paper concludes no increased risk of autism following exposure to wild measles and vaccinations W. CHEN, S. LANDAU, P. SHAM and E. FOMBONNE Psychological Medicine (April 2004), Cambridge University Press 34:543-553 Paper examines whether, in the UK, there is an increased risk of autism (AD) following exposures, in early life, to wild measles, live attenuated measles, alone or in combination as MMR, and the alteration of the mumps strain within MMR. The paper concludes no increased risk of autism (AD) following exposures to wild measles and vaccinations with monovalent measles, and Urabe or Jeryl-Lynn variants of MMR, were detected. To view an abstract of this paper please go to: http://journals.cambridge.org/bin/bladerunner?REQUNIQ=1087906601&REQSESS=341067&117000REQEVENT=&REQINT1=211198&REQAUTH=0 Original article : http://www.mmrthefacts.nhs.uk/news/newsitem.php?id=65 MMR news 12-Dec-03: No increase in autism prevalence associated with the use of the MMR vaccine Study shows no proof that the overall risk of autism is higher in children who were vaccinated with MMR Miller E (July 2003) Measles-mumps-rubella vaccine and the development of autism, Seminars in Pediatric Infectious Diseases 14:No.3: 199-206 The measles-mumps-rubella (MMR) vaccine has been postulated to cause a form of autism characterized by regression and bowel symptoms, and onset occurring shortly after vaccination. It is also claimed that, as a result, there has been a dramatic increase in autism prevalence. These hypotheses have now been tested in a number of epidemiologic studies that are reviewed in this article. None has found any evidence of the existence of a phenotypically distinct form of autism in children who received the MMR vaccine or of a clustering of onset symptoms in children who are autistic after receiving the MMR vaccine. There is no proof that the overall risk of autism is higher in children who were vaccinated with MMR or of an increase in autism prevalence associated with the use of the MMR vaccine. No epidemiologic evidence suggests an association between MMR vaccination and autism. Moreover, epidemiologic evidence against such an association is compelling. http://www2.us.elsevierhealth.com/script… (Long link) (Registration required for full text) Original article : http://www.mmrthefacts.nhs.uk/news/newsitem.php?id=68 MMR news 10-Feb-04: MMR Vaccine and Autism: An Update of the Scientific Evidence Evidence favours the rejection of a causal relationship between MMR and autistic spectrum disorder Frank DeStefano and William W Thompson (Feb 2004) MMR Vaccine and Autism: An Update of the Scientific Evidence Expert Review of Vaccines 3(1):19-22(2004) Update of scientific evidence in published studies have continued not to find an increased risk of autistic spectrum disorder associated with MMR. MMR vaccine also has not been found to be associated with a unique syndrome of developmental regression and gastrointestinal disorders. There is convincing evidence that MMR does not cause autism or any particular subtypes of autistic spectrum disorder. To read a summary of this report: http://www.future-drugs.com/summery.asp?… (Long link) For full report or pdf subscription is required. Original article : http://aapnews.aappublications.org/cgi/content/full/e2004128v1 NEWS AND FEATURES IOM report: Thimerosal, MMR vaccine not linked to autism Neither thimerosal nor the measles-mumps-rubella (MMR) vaccine is associated with autism, according to a new report from the Institute of Medicine (IOM) of the National Academies Immunization Safety Review Committee. Further, the hypotheses regarding how the MMR vaccine and thimerosal could trigger autism lack supporting evidence and are theoretical only. The report, Vaccines and Autism, is based on a thorough review of clinical and epidemiological studies and updates two earlier IOM reports, published in 2001. At that time, it was determined that the evidence did not show an association between the MMR vaccine and autism, but there was not enough evidence to determine whether thimerosal was associated with neurodevelopmental disorders such as autism. The committee also reviewed evidence related to possible biological mechanisms by which immunizations might trigger autism, but said no evidence has yet been found that the immune system or its activation play a role in causing autism. It reaffirms a previous recommendation to conduct studies to identify risk factors and biological markers of autism spectrum disorders (ASD) in order to better understand genetic and environmental causes of ASD. Today, with the exception of some flu vaccines, vaccines routinely given to young children either don’t contain thimerosal or have trace amounts. Vaccine manufacturers are working to remove thimerosal from those flu vaccines that still contain the preservative. The study is the eighth and final in a series on vaccine safety conducted by the IOM, a private, nonprofit institution that provides health policy advice under a congressional charter granted to the National Academy of Sciences. The report is available on the National Academies Press Web site. Daftar vaksin yang mengandung thiomersal dapat dilihat di: http://www.vaccinesafety.edu/thi-table.htm Menurut ahlinya DR. drg Julia Maria (Pakar Antropologi asal Indonesia yang bermukim di Beelanda) Jadi kalau kita ikuti terus, di dunia ini timbul 3 aliran besar: 1) yang menggunakan pendekatan multidisplin dalam penegakan diagnosa dengan pendekatan psikologi & pedagogi dalam penangannya, serta menggunakan pendekatan individual. Kelompok ini adalah kelompok mainstream ilmiah. 2) yang melihat bahwa berbagai gangguan bisa ditreat dengan beberapa model terapi perilaku dan sensori (nonbiomedical treatment), pendekatan non multidisiplin dalam penegakan diagnosa. 3) yang melihat bahwa berbagai gangguan itu bisa ditreat dengan biomedical (penggunaan probiotik, hormon, food supplement, garam nineral, anti oksidan, dlsb). 2) & 3) lebih kepada alternative medicine, tapi yang ngerjakan juga dokter & psikolog (profesional). Masing-masing kelompok melansir teori-teorinya, yang ujungnya yang klenger masyarakat luas, karena tidak tahu lagi mana yang benar. Jadi sampai saat ini para ahli lebih menekankan bahwa gangguan autism berada di dalam gene. Sekalipun kromosom mana yang mempengaruhi terjadinya gangguan autism masih belum diketahui secara pasti (karena menyangkut setidaknya ada 12 kromosom – dan penelitiannya belum selesai) tetapi dari berbagai penelitian kembar identik menunjukkan kemungkinan terjadinya autism jauh lebih besar secara siknifikan bila dibandingkan dengan nonidentik twins. http://www.nichd.nih.gov/publications/pubs/upload/autism_genes_2005.pdf

Peneliti Vaksin-Autisme Dinilai Melanggar

Selasa, 2 Februari 2010 | 03:33 WIB

LONDON, MINGGU – Andrew Wakefield, dokter yang mengaitkan vaksin dengan autisme dan kelainan perut pada anak, belakangan ini menuai kontroversi. Kali ini kritik terkait dengan pelanggaran etika yang dilakukan Andrew tentang proses penelitiannya tersebut.

The General Medical Council menyatakan, dokter tersebut tidak jujur dan tidak bertanggung jawab selama penelitian. Dia dicap tak berperasaan terhadap anak-anak yang terlibat dalam studi tersebut.

Pada 1998, Wakefield (ahli sistem pencernaan) di London’s Royal Free Hospital memublikasikan sebuah studi menggemparkan di jurnal Lancet. Studi itu mengaitkan vaksin Measles, Mumps and Rubella (MMR) dengan autisme dan gangguan pencernaan pada anak. Vaksin itu untuk mencegah penyakit demam campak, beguk, dan rubela. Andrew juga membuat sejumlah pernyataan agar orangtua menolak vaksin MMR. Akibatnya, cakupan vaksinasi menurun, dari sekitar 90 persen pada pertengahan 1990-an menjadi di bawah 70 persen.

The General Medical Council, lembaga yang mengurusi registrasi dan regulasi dokter di Inggris, tengah mempertimbangkan mencabut izin praktik Wakefield. Lembaga itu menggarisbawahi beberapa tindakan Wakefield yang merugikan hak anak yang terlibat dalam studi tahun 1998. Wakefield dianggap melakukan tes invansif terhadap anak seperti kolonoskopi dan pengumpulan cairan otak dan sumsum belakang tanpa mempertimbangkan efeknya terhadap anak. Metode Wakefield mengambil sampel darah juga menuai kritik. Wakefield dianggap membayar 8 dollar AS kepada anak-anak yang hadir dalam pesta ulang tahun putranya untuk menyumbangkan darah mereka.

Wakefield yang kini Executive Director Thoughtful House, sebuah pusat riset autisme di Austin, Texas, menganggap keputusan itu tidak berdasar dan tidak adil. Dia menyatakan tidak menyesal terhadap penelitian yang dilakukannya itu. Dia masih mendapat dukungan dari sejumlah orangtua. (TIME/INE)

 Sumber : Kompas

Hari ini, Kamis 8 Maret 2010 saya kembali terusik dengan artikel yang di publish Kompas sbb:

Deteksi Kadar Merkuri Lewat Analisa Rambut

Kamis, 8 April 2010 | 09:02 WIB

JAKARTA, KOMPAS.com – Sejauh ini, belum diketahui pasti penyebab autisme. Salah satu konsep mengatakan gejala autisme timbul akibat racun-racun dari lingkungan atau logam berat yang tidak bisa dibersihkan karena anak memiliki kelemahan genetik.

Untuk mendeteksi kadar logam berat dalam tubuh si anak, tersedia analisa tes rambut untuk menghitung nutrisi dan kadar racun mineral. “Tingkat dari racun dan nutrisi mineral bisa dipakai untuk mendiagnosa kelainan perilaku pada anak-anak autis,” kata Dr.Igor Tabrizian, pakar analisa rambut dari Australia dalam sebuah seminar mengenai autis beberapa waktu lalu di Jakarta.

Di dalam rambut, kuku dan gigi, mineral-mineral dalam bentuk kecil disimpan. Ini karena struktur rambut tidak berubah sehingga mineral yang tertanam dalam rambut dan kadarnya tidak berubah meski rambut memanjang. “Rambut manusia adalah rekaman sejarah yang bisa merefleksikan perubahan metabolisme,” tambah Igor.

Pemeriksaan melalui tes darah dianggap kurang akurat karena logam berat akan hilang dalam beberapa jam dan dikeluarkan tubuh. Demikian juga halnya dengan tse urine karena hanya mencerminkan kadar logam berat yang dilepaskan oleh darah oleh ginjal untuk jangka pendek.

Analisa rambut dilakukan dengan mengumpulkan sampel rambut si anak. Dibutuhkan kira-kira 600 miligram rambut untuk mengetahui 17 logam berat beracun dan 23 elemen penting.

Menurut Igor, kunci keakuratan analisa rambut terletak pada kredibilitas laboratorium dan keahlian ahli medis dalam menginterpretasikan hasil analisa.

Untuk saat ini, analisa tes rambut belum dapat dilakukan di Indonesia. Para orangtua yang ingin melakukan analisa rambut perlu mengirimkan sampel rambut ke Amerika Serikat atau Australia dengan biaya relatif mahal, mencapai 125 dollar AS, belum termasuk ongkos kirim.

Sumber : Kompas

Dan ini

 

Detoks Pengusir Racun Logam pada Anak Autis
Kamis, 8 April 2010 | 09:15 WIB

JAKARTA, KOMPAS.com – Anak-anak autis biasanya mengalami alergi dan MEMILIKI kondisi pencernaan yang jelek. Sekitar 88 persen anak autis memiliki kondisi usus rusak (autistic colistic). Ada kecurigaan mereka mengalami keracunan logam berat.

Pakar analisa rambut dari Australia, Dr.Igor Tabrizian, mengatakan, logam berat dalam tubuh anak autis baru bisa dikeluarkan melalui proses detoks. “Sebelum mengetahui program detoks yang tepat, perlu diketahui dulu tingkat keracunan yang dialami anak,” paparnya dalam sebuah seminar autis ‘Menyambut Hari Autisme Sedunia 2010′ di Jakarta beberapa waktu lalu.

Analisa rambut dapat dilakukan untuk mengidentifikasi kekurangan nutrisi jangka panjang yang merupakan akar dari penyakit yang ada, serta menemukan logam berat beracun yang bisa mencetuskan penyakit.

Proses pembuangan racun (detoks), menurut Igor, dilakukan dengan pemberian suplemen yang dibagi menjadi beberapa kategori, yakni memperbaiki, memberi nutrisi esensial, pembersih racun, serta memperbaiki neurotransmitter.

Nutrisi yang mampu memperbaiki antara lain zinc, aloe vera, prebiotik dan probiotik, vitamin E, zat besi, magnesium, vitamin E, dan vitamin B. Program detoks ini dilakukan selama 6-48 bulan, tergantung derajat keparahan logam berat yang menumpuk.

Sebelum pemberian suplemen detoks, masalah pencernaan anak autis sebaiknya diperbaiki dengan cara melakukan pantang produk gluten atau tepung dan produk susu. Menurut Igor, sistem pencernaan pada anak autis tidak dapat memisahkan protein, sehingga beberapa jenis asam amino justru bergabung.

“Reaksi penggabungan ini akan ditangkap otak seperti narkotik sehingga menimbulkan halusinasi dan menimbulkan gangguan perilaku, akibatnya anak menjadi hiperaktif,” paparnya.

Untuk mengetahui tingkat keberhasilan proses detoks ini, orangtua bisa melakukan analisa rambut secara berkala. “Selama proses pembuangan racun, kadar polutan dalam tubuh anak akan naik turun. Jadi tak perlu kaget jika hasilnya menunjukkan kadar logam beratnya masih tinggi,” katanya.

Sumber : Kompas

 

Berikut informasi pembanding yang dapat saya sampaikan :

 

Commercial Hair Analysis:
A Cardinal Sign of Quackery

Stephen Barrett, M.D.

Hair analysis is a test in which a sample of a person’s hair—typically from the back of the neck—is sent to a laboratory for measurement of its mineral content. This discussion concerns multielemental hair analysis in which a single test is used to determine values for many minerals simultaneously. This type of analysis used by chiropractors, “nutrition consultants,” physicians who do chelation therapy, and other dubious practitioners who claim that hair analyses can help them diagnose a wide variety of diseases and can be used as the basis for prescribing supplements.

Analysis of Proponent Claims

Proponents of hair analysis claim that it is useful for evaluating a person’s general state of nutrition and health and is valuable in detecting predisposition to disease. They also claim that hair analysis enables a doctor to determine if mineral deficiency, mineral imbalance or heavy metal pollutants in the body may be the cause of a patient’s symptoms. These claims are false.

  • Hair analysis is not reliable for evaluating the nutritional status of individuals. In 1974, the AMA Committee on Cutaneous Health and Cosmetics noted: “The state of health of the body may be entirely unrelated to the physical and chemical condition of the hair . . . Although severe deficiency states of an essential element are often associated with low concentrations of the element in hair, there are no data that indicate that low concentrations of an element signify low tissue levels nor that high concentrations reflect high tissue stores. Therefore . . . hair metal levels would rarely help a physician select effective treatment.”
  • Most commercial hair analysis laboratories have not validated their analytical techniques by checking them against standard reference materials. The techniques typically used to prepare samples for analysis can introduce errors for many of the elements being determined.
  • Hair mineral content can be affected by exposure to various substances such as shampoos, bleaches and hair dyes. No analytic technique enables reliable determination of the source of specific levels of elements in hair as bodily or environmental.
  • The level of certain minerals can be affected by the color, diameter and rate of growth of an individual’s hair, the season of the year, the geographic location, and the age and gender of the individual.
  • Normal ranges of hair minerals have not been defined.
  • For most elements, no correlation has been established between hair level and other known indicators of nutrition status. It is possible for hair concentration of an element (zinc, for example) to be high even though deficiency exists in the body.
  • Hair grows slowly (1 cm/month), so even hair closest to the scalp is several weeks old and thus may not reflect current body conditions for purposes of health diagnosis.
  • The use of a single multielemental hair analysis test as the sole means of diagnosis violates basic tenets of medical practice that laboratory findings should be considered together with the patient’s history and physical examination, and that the practitioner should keep in mind that laboratory errors occur.

For these reasons, multielemental analysis of human hair is not a valid technique for identifying an individual’s current bodily excesses or deficiencies of essential or nonessential elements. Nor does it provide a valid basis for recommending vitamins, minerals, or other dietary supplements [2,3]

In the mid-1980s, about 18 laboratories were doing commercial hair analysis in the United States. Today there are fewer. Some laboratories have belonged to the American Society of Elemental Testing Laboratories (ASETL). In 1982, ASETL began a program in which a well-known proficiency-testing service received and tabulated the data from analyses of identical hair samples sent to seven member laboratories. However, at the end of the year, the testing service refused to continue because the data were inconsistent and appeared to have no clinical significance.

In 1983 and 1984, I sent hair samples from two healthy teenagers to 13 of the commercial laboratories [4]. In 1985, I sent paired samples from one of the girls to five more labs. The reported levels of most minerals varied considerably between identical samples sent to the same laboratory, and from laboratory to laboratory. The laboratories also disagreed about what is “normal” or “usual” for many of the minerals, so that a given mineral value might be considered low by some laboratories, normal by others and high by others.

Most of the reports contained computerized interpretations that were voluminous and potentially frightening to patients. The nine labs that included supplement advice in their reports suggested them every time, but the types and amounts varied widely from report to report and from lab to lab. Many of the items recommended were bizarre mixtures of vitamins, minerals, nonessential food substances, enzymes, and extracts of animal organs. One report diagnosed 23 “possible or probable conditions,” including atherosclerosis and kidney failure, and recommended 56 supplement doses per day. Literature from most of the laboratories suggested that their reports were useful in managing a wide variety of diseases and supposed nutrient imbalances. I concluded that commercial use of hair analysis in this manner is unscientific, economically wasteful, and probably illegal, and that even if hair analysis were a valuable diagnostic tool, it is doubtful whether the laboratory reports themselves were reliable.

In 1985, the public affairs committee of the American Institute of Nutrition/American Society for Clinical Nutrition issued a position paper on hair analysis. The paper concluded that although hair analysis may have some value for comparing population groups as to status of various minerals or assessing exposure to heavy metals, assessment of individual subjects appears to have “almost insurmountable difficulties.” For this reason, said the paper, hair analysis might best be reserved for experimental studies designed to evaluate its potential as an indicator of nutrition status and perhaps for some public health surveys. Noting that about 100 articles a year were published on hair analysis, one nutritionist who reviewed the position paper suggested that the test’s inherent limitations made much of the research useless [5].

The AMA’s current policy on hair analysis—adopted in 1984 and reaffirmed in 1994, is:

The AMA opposes chemical analysis of the hair as a determinant of the need for medical therapy and supports informing the American public and appropriate governmental agencies of this unproven practice and its potential for health care fraud [6].

Some hair analysis proponents claim that hair analysis can detect allergies. The claim is completely senseless. In 1987, the Lancet published a study in which the ability to diagnose allergic disease was studied in 9 fish-allergic and 9 control subjects, who provided specimens of blood and hair for testing. All fish-allergic subjects had previously been shown at Guy’s Hospital to have a positive skin prick test to fish. The specimens were submitted as coded, duplicate samples to five commercial laboratories that offered to test for allergy. All five laboratories were not only unable to diagnose fish allergy but also reported many allergies in apparently non-allergic subjects and provided inconsistent results on duplicate samples from the same subject [7].

A subsequent 2-year study of students exposed to fumes from metal welding found that hair analysis did not consistently reflect blood levels of 11 heavy metals [8].

In 1999, researchers from the California Department of Health located nine laboratories and sent identical samples to six of them. The reported mineral levels, the alleged significance of the findings, and the recommendations made in the reports differed widely from one to another. The researchers concluded that the procedure is still unreliable and recommended that government agencies act vigorously to protect consumers [9]. An editorial accompanying this report in JAMA provided additional information about why hair analysis cannot provide a reliable basis for “nutritional counseling.” [10]

In 2001, German researchers did a study similar to mine in which they sent hair samples from two volunteers to seven commercial hair analysis laboratories. They found inconsistencies in both both the results and the laboratory reference ranges and concluded that “hair mineral analysis from these laboratories is unreliable.” [11]

Insurance companies do not knowingly cover the use of hair analysis for nutritional analysis. Aetna, for example, considers chemical hair analysis “experimental and investigational, except for diagnosis of suspected chronic arsenic poisoning.” [12] CIGNA does not cover it for any reason [13]. A recent review concluded that determination of arsenic in hair and nails has been most useful in epidemiological studies performed to evaluate environmental exposures of populations to inorganic arsenic but is less useful in the evaluation of an individual patient [14].

Government Actions

Hair analysis was involved in a case prosecuted in 1980 by the Los Angeles City Attorney’s Office. According to the official press release, Benjamin Colimore and his wife, Sarah, owners of a health-food store, would take hair samples from customers in order to diagnose and treat various conditions. Prosecution was initiated after a customer complained that the Colimores had said she had a bad heart valve and was suffering from abscesses of the pancreas, arsenic in her system, and benign growths of the liver, intestine, and stomach-all based on analysis of her hair. Two substances were prescribed, an “herbal tea” which turned out to be only milk sugar, and “Arsenicum,” another milk-sugar product that contained traces of arsenic. Another sample of hair was taken when the customer returned to the store five weeks later. She was told that the earlier conditions were gone, but that she now had lead in her stomach. A government investigator received similar diagnosis and treatment. After pleading “no contest” to one count of practicing medicine without a license, the Colimores were fined $2,000, given a sixty-day suspended jail sentence, and placed on probation for two years.

In 1985, in response to a petition by the Federal Trade Commission (FTC), a federal judge issued a permanent injunction against Arthur, Ethel and Alan Furman and any business through which they might act. The order forbids “holding themselves out . . . to persons other than health professionals, as being able, on the basis of hair analysis, to measure accurately the elemental content of a person’s body or to recommend vitamin, mineral or other dietary supplements which can correct chemical excesses and deficiencies in a person’s body.” [15] As a result of the FTC action, the Furmans’ laboratory closed and, until the Internet became popular, direct advertising to the public was rare. However, the FTC has ignored the laboratories that serve practitioners because it feels that practitioner misconduct should be regulated by state agencies.

In 1986, Analytical Research Laboratories (ARL) of Phoenix, Arizona signed a consent agreement with the New York State Attorney General to stop “soliciting and accepting hair specimens for laboratory examination where the purpose is to determine possible excesses of deficiencies in nutrient mineral levels or toxic metal levels in the body.” The Attorney General acted because a health food store proprietor had been using hair analysis as the basis for recommending vitamin and mineral supplements. ARL had not been licensed to operate within New York State, and hair analysis for the purpose of determining nutrient levels is not legal there.

In 1986, Doctor’s Data, a Chicago-based laboratory agreed to stop accepting human hair specimens from New York State unless it can obtain a permit from the New York State Department of Health [16]. The company also agreed to pay $25,000 in costs and penalties [17]. Action was taken because a bogus “nutrition consultant” had been using the test as a basis for prescribing vitamins, minerals, and other supplements.

A Sampling of Internet Claims

Biochemical Laboratories, of Edgewood, New Mexico, claimed that abdominal pain, hypertension, anemia, hypoglycemia, anxiety, impotence, depression, infertility, diarrhea, joint pain, learning, disorders, fatigue, headache, and premenstrual syndrome all result from “chronic metal imbalances,” which, presumably, can be diagnosed with hair analysis and treated with dietary supplements.

Trace Elements, Inc., of Dallas, Texas, has promoted “balancing body chemistry through hair tissue mineral analysis.” The company claims to have developed “a precise nutritional therapeutic approach based on the recognition of eight individual biochemical types using elemental analysis of hair.” It has also sold “metabolic supplements synergistically formulated” for each of these types. It markets primarily through chiropractors.

Trace Mineral Systems, of Alexandria, Virginia, touted its hair analysis as “the test that helps body chemistry” and markets it directly to the public. A recent magazine ad claimed that its test reports would show “the body’s excesses, deficiencies & toxicities and the diseases associated with them.” [18]

Doctor’s Data reports the level of a “toxic mineral” as high when the amount is near the top of its “reference range.” This merely means that the specimen contained more than most other specimens handled by the lab. It does not mean that the level is abnormal or that the level within the patient’s body is dangerous. In a recent paper, the company acknowledged that “compared to interpretation of commonly measured analyses in blood or serum, interpretation of elemental analyses from hair seems primitive.” Despite, this, the authors claimed that it would be prudent to “adopt a reference range consistent with what is observed in 95% of a healthy population.” [19]

The Bottom Line

Hair analysis is worthless for assessing the body’s nutritional status or serving as a basis for dietary or supplement recommendations. Should you encounter a practitioner who claims otherwise, run for the nearest exit and file a complaint with your state attorney general!

For Additional Information

References

  1. Lazar P. Hair analysis: What does it tell us? JAMA 229:1908-1909, 1974.
  2. Hambidge KM. Hair analyses: Worthless for vitamins, limited for minerals. American Journal of Clinical Nutrition 36:943-949, 1983.
  3. Klevay LM and others. Hair analysis in clinical and experimental medicine. American Journal of Clinical Nutrition 46:233-236, 1987.
  4. Barrett S. Commercial hair analysis: Science or scam? JAMA 254:1041-1045, 1985.
  5. Fosmire GJ et al. Hair analysis to assess nutritional status. AIN Nutrition Notes 21(4):10-11, 1985.
  6. Hair analysis: A potential for medical abuse. Policy number H-175.995,(Sub. Res. 67, I-84; Reaffirmed by CLRPD Rep. 3 – I-94)
  7. Sethi TJ and others. How reliable are commercial allergy tests? Lancet Jan 10;1(8524):92-94, 1987.
  8. Teresa M and others. Trace-element concentration in blood and hair of young apprentices of a technical-professional school. The Science of the Total Environment 205:189-193, 1997.
  9. Seidel S and others. Assessment of commercial laboratories performing hair mineral analysis. JAMA 285:67-72, 2001.
  10. Steindel SJ, Howanitz PJ. The uncertainty of hair analysis for trace minerals. JAMA 285:83-85, 1999.
  11. Drasch G, Roider G. Assessment of hair mineral analysis commercially offered in Germany. Journal of Trace Elements in Medical Biology 16:27-31, 2002.
  12. Aetna clinical policy bulletin on hair analysis. Revised June 17, 2008.
  13. CIGNA HealthCare coverage position statement: Chemical hair analysis. Revised Feb 15, 2008.
  14. Goldman RH. Arsenic exposure and poisoning. Waltham, MA: UpToDate, 2008.
  15. FTC v Furman, 1985-1 CCH Trade Case (CCH) ¶66486 (ED Va 1985).
  16. Consent judgment. New York v Doctor’s Data Laboratories, Index No. 42127/85, filed Oct 16, 1986.
  17. Stipulation and judgment. New York v Doctor’s Data Laboratories, Index No. 42130/85, filed Oct 16, 1986.
  18. Trace Mineral Systems. Alternative Medicine Digest, Aug/Sept 1998, p 99.
  19. Druyan ME and others. Determination of reference ranges for elements in human scalp hair. Biological Trace Element Research 62:183-197, 1998.

This article was revised on November 21, 2008.

Sumber: Quackwatch.org

 

Dubious Mercury Testing

Robert Baratz, M.D., D.D.S., Ph.D.

Mercury is found in the earth’s crust and is ubiquitous in the environment. Thus, even without amalgam fillings, everyone has small but measurable blood and urine levels. Amalgam fillings raise these levels slightly, but this has no clinical significance.

The legal limit of safe mercury exposure for industrial workers is 50 micrograms per cubic meter of air for 8 hours per day and 50 weeks per year. Exposure at this level will produce urine mercury levels of about 135 micrograms per liter. These levels are much higher than those in the general public but produce no symptoms and are considered safe.

Most people without fillings have a maximum of 5-10 micrograms per liter of urine. Most practicing dentists have levels below 10 micrograms per liter, even though they are exposed to mercury vapor when placing or removing amalgam filings and typically have amalgams in their own teeth. Thus, even with that exposure, the maximum levels found in dentists are only twice those of their patients—and most dentists are have the same levels as most patients. These are far below the levels known to affect health, even in a minor way.

Despite these facts, small percentages of dentists, physicians, and chiropractors are advising patients to have their amalgam fillings replaced with other materials. Their advice is typically accompanied by one or more tests that are either misinterpreted or completely bogus. These activities are the hallmarks of a scam.

Breath Testing

Breath testing is done by asking the patient to chew gum vigorously for several minutes and then probing the mouth with an industrial mercury detector. These instruments measure changes in electrical conductivity caused by absorption of mercury or other metals onto a gold foil film. In the hands of anti-amalgam dentists, several factors combine to produce falsely high readings.

  • Vigorous chewing provokes a release of detectable but tiny quantities of mercury in the breath for a few minutes. Because people only chew during a small part of the day, the resultant readings are much higher than the average amounts released per 24 hours. The correct way to quantify mercury release (or potential absorption) is to determine the average amount over a 24-hour period.
  • The devices suck in the air so that any metallic vapor and various other compounds are deposited on a gold film. The electrical resistance of the film is measured and interpreted. The volume of the mouth is 100 to 200 cubic centimeters. The device is designed to measure a volume of air several times the capacity of the mouth. When applied to the mouth, it creates a vacuum that causes mercury to be released from the fillings, leading the machine to give an artificially high reading. This reflects not only more mercury than would normally be present, but also other substances (including copper, silver, tin, plastics, foods, and gasses produced by bacteria), which also deposit on the film and change its electrical resistance. Typically the patient is shown how high the needle has gone and told that this number indicates mercury poisoning. Small errors in measurement, or large errors produced by the multiple sampling of the same volume, compound the problem.
  • To ensure accuracy, these machines should be calibrated by testing them with standard concentrations of mercury. This is important because over time, the build-up of substances on the gold film tends to raise the readings. Anti-amalgam dentists almost never calibrate their equipment to retain accuracy.

Urine Testing

Because mercury is ubiquitous, the body reaches a steady state in which tiny amounts are absorbed and excreted. Thus, it is common to find mercury in people’s urine. Mercury can also be found in the blood, because this is the major medium for transporting materials around the body. Large-scale population studies have shown that the general population has urine-mercury levels below 10 micrograms/liter. Industrial workers, and dentists, who have regular exposure to mercury vapor also have low values. Because urine-mercury levels represent the chronic, steady state, exposure to the body of mercury, they are fairly reliable indicators of past exposure, since they tend to even out the peaks and valleys of transient rises and falls in the blood level. Urine measurements should be performed on the first urine specimen of the day, which would be the most concentrated, or (preferably) on a 24-hour urine specimen.

Urine mercury levels can be artificially raised by administering a mercury scavenger (chelating agent) such as DMPS or DMSA, which collect the small amounts of mercury from the body, concentrate them, and then force them to be excreted. In other words, mercury that normally recirculates within the body is now bound and excreted. The urine level under such circumstances is artificially raised above the steady-state level. A study of urine mercury levels in people given DMSA or a placebo has found no association between the mercury levels and the number of dental amalgam surfaces [1]. The use of a chelating agent before testing—”provoked testing”—should be considered a scam. Anyone told that a urine-mercury level produced after taking DMPS represents a toxic state is being misled.

In February 2005, the State of Connecticut obtained a consent order barring psychiatrist Robban Sica, M.D., from using provoked testing to diagnose “heavy metal toxicity.” [2] It would be good if all state licensing boards did the same.

Blood Testing

Mercury is excreted by the kidneys, which filter the blood. The mercury levels of blood are lower than those of urine and therefore more difficult to detect. For this reason, blood testing for mercury is not commonly done. Even at high levels of mercury exposure, industrial workers show blood concentrations in the parts-per-billion range, typically less than 5 parts per billion. These are close to the limits of detection. In this range, the amounts are too small to identify the type of mercury or its source. Urine mercury testing gives a more meaningful picture of exposure and is also more accurate because the mercury is more concentrated.

Skin Testing

Skin testing for allergies is both an art and a science. Correct concentrations of a suspected offender must be correctly applied and interpreted. To be valid, patch testing must be done by a qualified tester using appropriate controls. Mercury patch testing is usually done with corrosive mercury salts that cause the skin to redden and possibly swell. Even very dilute concentrations can cause redness [2]. Anti-amalgamists misinterpret these signs of irritation as allergy or toxicity. So-called “positive” tests indicate only that the body can detect the substance. True allergy to mercury is very rare. Its symptoms are like those of any other allergy and include itching, rashes, and swelling. Allergic responses do not include “brain fog,” forgetfulness, or other nonspecific symptoms. Moreover, sensitivity to mercury might be the result of exposure to mercury from other sources, such as certain vaccine preparations, preservatives in cosmetics, or foods (most notably fish).

Stool Testing

No stool test for mercury has been standardized. Fecal mercury levels are not an accurate indicator of mercury exposure. The amount found in stool reflects the amount eaten and not absorbed plus anything excreted in the stool. Stool patterns (frequency, consistency, volume, and density) vary widely from person to person, and thus, the amount of mercury found in stool would be very hard to translate into to body burden, body stores, or excretion. Only about 5-10% of ionic mercury (the kind associated with most alleged poisonings) is absorbed from the gut. The main route of mercury excretion is through the kidneys into the urine, and not into the stool. Further, to make an analysis, ionic mercury must be separated from any organic mercury that occurs in foods, which is difficult to do. Thus, at best, a stool test might indicate that mercury entered the gastrointestinal tract, but it could not provide an accurate measurement of either exposure or what was absorbed into the body.

Hair Analysis

Hair mercury levels are not an accurate indicator of mercury exposure. Hair testing has never been standardized to provide meaningful information. In fact, it cannot be standardized because:

  • Traces of everything eaten, imbibed, or breathed can end up in the hair. While hair analysis may be of use for detecting substances—such as arsenic—that are not part of the normal environment, mercury is ubiquitous and is normally found in the hair, whether the person has mercury fillings or not. It gets there from food, water, and air.
  • Mercury can be accurately measured in blood and also in urine, which is a distillate of the blood serum. Hair is similar to the outer layer of the skin and has no blood supply. Thus the amount of mercury in hair does not reflect the concentration in the rest of the body. Measurements of blood and urine from thousands of people have never shown high levels of mercury in the general population. Only workers with high work exposure have shown abnormal levels in blood and urine, but these are not in the toxic range.
  • Hair grows at different rates in different individuals and its composition is quite variable. Measuring mercury means measuring an absolute amount that is compared to the weight of the whole hair; that is, determining the concentration, expressed as micrograms of mercury per gram of hair. However, the amount of a substance absorbed into the hair is influenced by surface area and hair composition. Since hair thickness, density, shape, and surface area vary from person to person, one cannot make a “standard” comparison.
  • Hair is subject to washing, shampoos, rinses, colorants, sun exposure, leaching from swimming and bathing, hair dryers, and a host of other treatments. Substances are regularly removed from the hair by these treatments, but the amounts removed are not known since the hair treatments are so varied. Similarly, other substances—including heavy metals—can actually be added by some of these processes. With some substances being added and others being removed, it is clear that the relative concentration of any particular substance, especially a metal, changes constantly and is thus uncertain..

Thus it should be obvious that analyzing hair for mercury is a waste of time and money and cannot be used to diagnose mercury poisoning. A competent practitioner would easily know this. It is fraudulent to use hair analysis to diagnose “toxic levels” of mercury (or any other heavy metal) or to assess nutritional status (and claim someone is “deficient” and prescribe or sell them supplements). Dr. Stephen Barrett calls commercial hair analysis “the cardinal sign of quackery.” [2]

Saliva Testing

Larry Clapp, a nonpracticing attorney who “coaches” people on how to deal with prostate cancer, prostate problems, and erectile problems, recommends that amalgam fillings be removed as part of his treatment system. In 2002 and 2003, he promoted an Immune Antibody Test,” a saliva test that he claimed would help guide “detoxification” after the removal of the fillings. During that period, his mercurytestkits.com Web site claimed that the test measured antibodies created by the immune system to deal with mercury in the tissues and that high readings were associated with serious illness. I am not aware of any such processes. The Web site site that advertised the test is no longer posted; and the lab that was doing it no longer offers it.

Electrodermal Testing

Some practitioners use quack diagnostic devices that are said to detect “electromagnetic imbalances.” One wire from the device goes to a brass cylinder covered by moist gauze, which the patient holds in one hand. A second wire is connected to a probe, which the operator touches to various points inside the mouth. This completes a low-voltage circuit, and the device registers the flow of current, which the operator misinterprets as abnormal.

References

  1. Frumkin H. Diagnostic chelation challenge with DMSA: A biomarker of long-term mercury exposure? Environmental Health Perspectives 109:167-171, 2001
  2. Consent agreement. In re: Robban Sica, M.D.. Petition No. 2002-0306-001-043, Feb 2005.
  3. Barrett S. Commercial hair analysis: A cardinal sign of quackery. Quackwatch, Jan 5, 2001.

This article was revised on February 19, 2005.

 

Sumber : quackwatch.org

 

Wassalam

Sumber : Ghozan Blog

From → Pro - Kontra

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