• Accupressure
• Accupuncture
• Adeli Suit
• Aminoacid Therapy
• Auditory Integration Training
• BioMed
• Conductive Education
• Cranial Sacral Therapy
• EEG Bio Feedback
• Felden Krais
• G-Therapy
• Horse Riding Therapy(Hippo Therapy)

• Hyperbaric Oxygen Therapy(HBO)
• Infant Massage Therapy
• Kinesiotaping
• Magnetic Therapy(Magnetic Energizing Method)
• Medek
• Rolfing
• Vojta Therapy
• Watsu
• Jin Shin
• Reiki
• Eureca

Bio Med

• Autism: a Novel Form of Mercury Poisoning
• Autoimmunity Testing in Autism
• Comprehensive Digestive Stool Analysis.pdf
• Dental Anesthesia for the Autistic Child
• Immune Panels For Autism Spectrum Children
• Labs and Testing Information
• Mercury Burden Study 2003.pdf
• Surgical Anesthesia and Autism

Summary Autism is a syndrome characterized by impairments in social relatedness and communication, repetitive behaviors, abnormal movements, and sensory dysfunction. Recent epidemiological studies suggest that autism may affect 1 in 150 U. S. children. Exposure to mercury can cause immune, sensory, neurological, motor, and behavioral dysfunctions similar to traits defining or associated with autism, and the similarities extend to neuroanatomy, neurotransmitters, and biochemistry. Thimerosal, a preservative added to many vaccines, has become a major source of mercury in children who, within their first two years, may have received a quantity of mercury that exceeds safety guidelines. A review of medical literature and U.S. government data suggests that

1. many cases of idiopathic autism are induced by early mercury exposure from thimerosal;
2. this type of autism represents an unrecognized mercurial syndrome; and
3. genetic and non-genetic factors establish a predisposition whereby thimerosal's adverse effects occur only in some children.

Introduction Autistic Spectrum Disorder (ASD) is a neurodevelopmental syndrome with onset prior to age 36 months. Diagnostic criteria consist of impairments in sociality and communication plus repetitive and stereotypic behaviors (1). Traits strongly associated with autism include movement disorders and sensory dysfunctions (2). Although autism may be apparent soon after birth, most autistic children experience at least several months, even a year or more of normal development -- followed by regression, defined as loss of function or failure to progress (2,3,4).

The neurotoxicity of mercury (Hg) has long been recognized (5). Primary data derive from victims of contaminated fish (Japan - Minamata Disease) or grain (Iraq, Guatemala, Russia); from acrodynia (Pink Disease) induced by Hg in teething powders; and from individual instances of mercury poisoning (HgP), many occurring in occupational settings (e.g., Mad Hatter's Disease). Animal and in vitro studies also provide insights into the mechanisms of Hg toxicity. More recently, the Food and Drug Administration (FDA) and the American Academy of Pediatrics (AAP) have determined that the typical amount of Hg injected into infants and toddlers via childhood immunizations has exceeded government safety guidelines on an individual (6) and cumulative vaccine basis (7). The mercury in vaccines derives from thimerosal (TMS), a preservative which is 49.6% ethylmercury (eHg) (7).

Past cases of HgP have presented with much inter-individual variation, depending on the dose, type of mercury, method of administration, duration of exposure, and individual sensitivity. Thus, while commonalities exist across the various instances of HgP, each set of variables has given rise to a different disease manifestation (8,9,10,11). It is hypothesized that the regressive form of autism represents another form of mercury poisoning, based on a thorough correspondence between autistic and HgP traits and physiological abnormalities, as well as on the known exposure to mercury through vaccines. Furthermore, other phenomena are consistent with a causal Hg-ASD relationship. These include (a) symptom onset shortly after immunization; (b) ASD prevalence increases corresponding to vaccination increases; (c) similar sex ratios of affected individuals; (d) a high heritability rate for autism paralleling a genetic predisposition to Hg sensitivity at low doses; and (e) parental reports of autistic children with elevated Hg.

Trait Comparison ASD manifests a constellation of symptoms with much inter-individual variation (3,4). A comparison of traits defining, nearly universal to, or commonly found in autism with those known to arise from mercury poisoning is given in Table I. The characteristics defining or strongly associated with autism are also more fully described.

Autism has been conceived primarily as a psychiatric condition; and two of its three diagnostic criteria are based upon the observable traits of

(a) impairments in sociality, most commonly social withdrawal or aloofness, and

(b) a variety of perseverative or stereotypic behaviors and the need for sameness, which strongly resemble obsessive- compulsive tendencies.

Differential diagnosis may include childhood schizophrenia, depression, obsessive-compulsive disorder (OCD), anxiety disorder, and other neuroses. Related behaviors commonly found in ASD individuals are irrational fears, poor eye contact, aggressive behaviors, temper tantrums, irritability, and inexplicable changes in mood (1,2,12-17). Mercury poisoning, when undetected, is often initially diagnosed as a psychiatric disorder (18). Commonly occurring symptoms include

(a) "extreme shyness," indifference to others, active avoidance of others, or "a desire to be alone";

(b) depression, "lack of interest" and "mental confusion;"

(c) irritability, aggression, and tantrums in children and adults;

(d) anxiety and fearfulness; and

(e) emotional lability.

Neuroses, including schizoid and obsessive-compulsive traits, problems in inhibition of perseveration, and stereotyped behaviors, have been reported in a number of cases; and lack of eye contact was observed in one 12 year old girl with mercury vapor poisoning (18-35).

The third diagnostic criterion for ASD is impairment in communication

1. Historically, about half of those with classic autism failed to develop meaningful speech
2. and articulation difficulties are common
3. Higher functioning individuals may have language fluency but still show semantic and pragmatic errors (3,36).

In many cases of ASD, verbal IQ is lower than performance IQ (3). Similarly, mercury-exposed children and adults show a marked difficulty with speech (9,19,37). In milder cases scores on language tests may be lower than those of unexposed controls (31,38). Iraqi children who were postnatally poisoned developed articulation problems, from slow, slurred word production to an inability to generate meaningful speech; while Iraqi babies exposed prenatally either failed to develop language or presented with severe language deficits in childhood (23,24,39). Workers with Mad Hatter's disease had word retrieval and articulation difficulties (21).

Nearly all cases of ASD and HgP involve disorders of physical movement (2,30,40). Clumsiness or lack of coordination has been described in many higher functioning ASD individuals (41). Infants and toddlers later diagnosed with autism may fail to crawl properly or may fall over while sitting or standing; and the movement disturbances typically occur on the right side of the body (42). Problems with intentional movement and imitation are common in ASD, as are a variety of unusual stereotypic behaviors such as toe walking, rocking, abnormal postures, choreiform movements, spinning; and hand flapping (2,3,43,44). Noteworthy because of similarities to autism are reports in Hg literature of

(a) children in Iraq and Japan who were unable to stand, sit, or crawl (34,39);
(b) Minamata disease patients whose movement disturbances were localized to one side of the body, and a girl exposed to Hg vapor who tended to fall to the right (18,34);
(c) flapping motions in an infant poisoned from contaminated pork (37) and in a man injected with thimerosal (27);
(d) choreiform movements in mercury vapor intoxication (19);
(e) toe walking in a moderately poisoned Minamata child (34);
(f) poor coordination and clumsiness among victims of acrodynia (45);
(g) rocking among infants with acrodynia (11); and
(h) unusual postures observed in both acrodynia and mercury vapor poisoning (11,31).

The presence of flapping motions in both diseases is of interest because it is such an unusual behavior that it has been recommended as a diagnostic marker for autism (46).

Virtually all ASD subjects show a variety of sensory abnormalities (2). Auditory deficits are present in a minority of individuals and can range from mild to profound hearing loss (2,47). Over- or under-reaction to sound is nearly universal (2,48), and deficits in language comprehension are often present (3). Pain sensitivity or insensitivity is common, as is a general aversion to touch; abnormal sensation in the extremities and mouth may also be present and has been detected even in toddlers under 12 months old (2,49). There may be a variety of visual disturbances, including sensitivity to light (2,50,51,52). As in autism, sensory issues are reported in virtually all instances of Hg toxicity (40). HgP can lead to mild to profound hearing loss (40); speech discrimination is especially impaired (9,34,). Iraqi babies exposed prenatally showed exaggerated reaction to noise (23), while in acrodynia, patients reported noise sensitivity (45). Abnormal sensation in the extremities and mouth is the most common sensory disturbance (25,28). Acrodynia sufferers and prenatally exposed Iraqi babies exhibited excessive pain when bumping limbs and an aversion to touch (23,24,45,53). A range of visual problems has been reported, including photophobia (18,23,34).

Comparison of Biological Abnormalities

The biological abnormalities commonly found in autism are listed in Table II, along with the corresponding pathologies arising from mercury exposure. Especially noteworthy similarities are described.

Autism is a neurodevelopmental disorder which has been characterized as "a disorder of neuronal organization, that is, the development of the dentritic tree, synaptogenesis, and the development of the complex connectivity within and between brain regions" (54). Depressed expression of neural cell adhesion molecules (NCAMs), which are critical during brain development for proper synaptic structuring, has been found in one study of autism (55). Organic mercury, which readily crosses the blood-brain barrier, preferentially targets nerve cells and nerve fibers (56); primates accumulate the highest Hg-levels in the brain relative to other organs (40). Furthermore, although most cells respond to mercurial injury by modulating levels of glutathione (GSH), metallothionein, hemoxygenase, and other stress proteins, neurons tend to be "markedly deficient in these responses" and thus are less able to remove Hg and more prone to Hg-induced injury (56). In the developing brain, mercury interferes with neuronal migration, depresses cell division, disrupts microtubule function, and reduces NCAMs (28, 57-59).

While damage has been observed in a number of brain areas in autism, many nuclei and functions are spared (36). HgP's damage is similarly selective (40). Numerous studies link autism with neuronal atypicalities within the amygdala, hippocampi, basal ganglia, the Purkinje and granule cells of the cerebellum, brainstem, basal ganglia, and cerebral cortex (36,60-69). Each of these areas can be affected by HgP (10,34,40,70-73). Migration of Hg, including eHg, into the amygdala is particularly noteworthy, because in primates this brain region has neurons specific for eye contact (74) and it is implicated in autism and in social behaviors (65,66,75).

Autistic brains show neurotransmitter irregularities which are virtually identical to those arising from Hg exposure: both high or low serotonin and dopamine, depending on the subjects studied; elevated epinephrine and norepinephrine in plasma and brain; elevated glutamate; and acetylcholine deficiency in hippocampus (2,21,76-83).

Gillberg and Coleman (2) estimate that 35-45% of autistics eventually develop epilepsy. A recent MEG study reported epileptiform activity in 82% of 50 regressive autistic children; in another study, half the autistic children expressed abnormal EEG activity during sleep (84). Autistic EEG abnormalities tend to be non-specific and have a variety of patterns (85). Unusual epileptiform activity has been found in a number of mercury poisoning cases (18,27,34,86-88). Early mHg exposure enhances tendencies toward epileptiform activity with a reduced level of seizure-discharge amplitude (89), a finding consistent with the subtlety of seizures in many autism spectrum children (84,85). The fact that Hg increases extracellular glutamate would also contribute to epileptiform activity (90).

Some autistic children show a low capacity to oxidize sulfur compounds and low levels of sulfate (91,92). These findings may be linked with HgP because (a) Hg preferentially binds to sulfhydryl molecules (-SH) such as cysteine and GSH, thereby impairing various cellular functions (40), and (b) mercury can irreversibly block the sulfate transporter NaSi cotransporter NaSi-1, present in kidneys and intestines, thus reducing sulfate absorption (93). Besides low sulfate, many autistics have low GSH levels, abnormal GSH-peroxidase activity within erythrocytes, and decreased hepatic ability to detoxify xenobiotics (91,94,95). GSH participates in cellular detoxification of heavy metals (96); hepatic GSH is a primary substrate for organic-Hg clearance from the human (40); and intraneuronal GSH participates in various protective responses against Hg in the CNS (56). By preferentially binding with GSH, preventing absorption of sulfate, or inhibiting the enzymes of glutathione metabolism (97), Hg might diminish GSH bioavailability. Low GSH can also derive from chronic infection (98,99), which would be more likely in the presence of immune impairments arising from mercury (100). Furthermore, mercury disrupts purine and pyrimidine metabolism (97,10). Altered purine or pyrimidine metabolism can induce autistic features and classical autism (2,101,102), suggesting another mechanism by which Hg can contribute to autistic traits.

Autistics are more likely to have allergies, asthma, selective IgA deficiency (sIgAd), enhanced expression of HLA-DR antigen, and an absence of interleukin-2 receptors, as well as familial autoimmunity and a variety of autoimmune phenomena. These include elevated serum IgG and ANA titers, IgM and IgG brain antibodies, and myelin basic protein (MBP) antibodies (103-110). Similarly, atypical responses to Hg have been ascribed to allergic or autoimmune reactions (8), and genetic predisposition to such reactions may explain why Hg sensitivity varies so widely by individual (88,111). Children who developed acrodynia were more likely to have asthma and other allergies (11); IgG brain autoantibodies, MBP, and ANA have been found in HgP subjects (18,111,112); and mice genetically prone to develop autoimmune diseases "are highly susceptible to mercury-induced immunopathological alterations" even at the lowest doses (113). Additionally, many autistics have reduced natural killer cell (NK) function, as well as immune-cell subsets shifted in a Th2 direction and increased urine neopterin levels, indicating immune system activiation (103,114-116). Depending upon genetic predisposition, Hg can induce immune activation, an expansion of Th2 subsets, and decreased NK activity (117-120).

Population Characteristics

In most affected children, autistic symptoms emerge gradually, although there are cases of sudden onset (3). The earliest abnormalities have been detected in 4 month olds and consist of subtle movement disturbances; subtle motor-sensory disturbances have been observed in 9 month olds (49). More overt speech and hearing difficulties become noticeable to parents and pediatricians between 12 and 18 months (2). TMS vaccines have been given in repeated intervals starting from infancy and continuing until 12 to 18 months. While HgP symptoms, may arise suddenly in especially sensitive individuals (11), usually there is a preclinical "silent stage" in which subtle neurological changes are occuring (121) and then a gradual emergence of symptoms. The first symptoms are typically sensory- and motor-related, which are followed by speech and hearing deficits, and finally the full array of HgP characteristics (40). Thus, both the timing and nature of symptom emergence in ASD are fully consistent with a vaccinal Hg etiology. This parallel is reinforced by parental reports of excessive amounts of mercury in urine or hair from younger autistic children, as well as some improvement in symptoms with standard chelation therapy (122).

The discovery and rise in prevalence of ASD mirrors the introduction and spread of TMS in vaccines. Autism was first described in 1943 among children born in the 1930s (123). Thimerosal was first introduced into vaccines in the 1930s (7). In studies conducted prior to 1970, autism prevalence was estimated, at 1 in 2000; in studies from 1970 to 1990 it averaged 1 in 1000 (124). This was a period of increased vaccination rates of the TMS- containing DPT vaccines among children in the developed world. In the early 1990s, the prevalence of autism was found to be 1 in 500 (125), and in 2000 the CDC found 1 in 150 children affected in one community, which was consistent with reports from other areas in the country (126). In the late 1980s and early 1990s, two new TMS vaccines, the HIB and Hepatitis B, were added to the recommended schedule (7).

Nearly all US children are immunized, yet only a small proportion develop autism. A pertinent characteristic of mercury is the great variability in its effects by individual, so that at the same exposure level, some will be affected severely while others will be asymptomatic (9,11,28). An example is acrodynia, which arose in the early 20th Century from mercury in teething powders and afflicted only 1 in 500-1000 children given the same low dose (28). Studies in mice as well as humans indicate that susceptibility to Hg effects arises from genetic status, in some cases including a propensity to autoimmune disorders (113,34,40). ASD exhibits a strong genetic component, with high concordance in monozygotic twins and a higher than expected incidence among siblings (4); autism is also more prevalent in families with autoimmune disorders (106).

Additionally, autism is more prevalent among boys than girls, with the ratio estimated at 4:1 (2). Mercury studies in mice and humans consistently report greater effects on males than females, except for kidney damage (57). At high doses, both sexes are affected equally; at low doses only males are affected (38,40,127).

Discussion

We have shown that every major characteristic of autism has been exhibited in at least several cases of documented mercury poisoning. Recently, the FDA and AAP have revealed that the amount of mercury given to infants from vaccinations has exceeded safety levels. The timing of mercury administration via vaccines coincides with the onset of autistic symptoms. Parental reports of autistic children with measurable mercury levels in hair and urine indicate a history of mercury exposure. Thus the standard primary criteria for a diagnosis of mercury poisoning - observable symptoms, known exposure at the time of symptom onset, and detectable levels in biologic samples (11,31) - have been met in autism. As such, mercury toxicity may be a significant etiological factor in at least some cases of regressive autism. Further, each known form of HgP in the past has resulted in a unique variation of mercurialism - e.g., Minamata disease, acrodynia, Mad Hatter's disease - none of which has been autism, suggesting that the Hg source which may be involved in ASD has not yet been characterized; given that most infants receive eHg via vaccines, and given that the effect on infants of eHg in vaccines has never been studied (129), vaccinal thimerosal should be considered a probable source. It is also possible that vaccinal eHg may be additive to a prenatal mercury load derived from maternal amalgams, immune globulin injections, or fish consumption, and environmental sources.

Conclusion

The history of acrodynia illustrates that a severe disorder, afflicting a small but significant percentage of children, can arise from a seemingly benign application of low doses of mercury. This review establishes the likelihood that Hg may likewise be etiologically significant in ASD, with the Hg derived from thimerosal in vaccines rather than teething powders. Due to the extensive parallels between autism and HgP, the likelihood of a causal relationship is great. Given this possibility, TMS should be removed from all childhood vaccines, and the mechanisms of Hg toxicity in autism should be thoroughly investigated. With perhaps 1 in 150 children now diagnosed with ASD, development of HgP-related treatments, such as chelation, would prove beneficial for this large and seemingly growing population.

Table I: Summary Comparison of Traits of Autism & Mercury Poisoning
(ASD references in bold; HgP references in italics)

Table II: Summary Comparison of Biological Abnormalities
in Autism & Mercury Exposure

References

Top of page

Autism, a developmental brain disorder, causes severe behavioral problems in children but it lasts a life-long. The cause and treatment of autism is not well known. We have studied autism as an autoimmune disorder. Autoimmunity is an abnormal condition in which a person's immune system goes haywire and reacts abnormally to his/her own organs. Thus autism will involve an autoimmune reaction to brain because brain is the affected organ. We have identified several autoimmune factors such as brain-specific autoantibodies, virus (and/or vaccine) serology, autoimmunity-producing cytokines, and serotonin and serotonin receptor antibodies. These factors are extremely important in identifying a virus-induced autoimmune pathology in autism. Therefore, the laboratory evaluation of these factors is helpful for uncovering a pathogenetic role of autoimmunity in autism and for monitoring patient responses before, during and after experimental immunotherapy that is known to produce significant improvements of clinical symptoms in children with autism.

[NOTE: Initially, I recommend Test numbers #1, #2 and #3 but you can choose whatever you like. All autistic patients (children and adults) should be tested].

1. Brain Autoantibody Test: This test measures antibodies to two brain proteins, namely myelin basic protein (MBP) and neuron-axon filament proteins (NAFP). Many autistic patients have these autoantibodies as a sign of autoimmunity to brain (Singh et al., 1993 & 1998; Singh 1999).
2. Virus Serology Test: This test assays for antibodies to measles virus (MV) and human herpesvirus-6 (HHV-6) that may be related to etiology of autism (Singh et al., 1998; Singh, 1999).
3. MMR Antibody Test: This test detects abnormal antibodies to MMR vaccine. Many autistic patients have these antibodies (Singh, 2000).
4. Cytokine Profile Test: This test measures two key cytokines, namely interleukin-12 (IL-12) and interferon-gamma (IFN-g). They are known to induce autoimmune diseases and are significantly elevated in autistic patients (Singh, 1996).
5. Serotonin and Serotonin Receptor Antibody Test: This test measures plasma/serum serotonin level and brain serotonin receptor antibody. Quite commonly, autistic patients have elevated levels of serotonin that may be related to serotonin receptor antibodies (Singh et al., 1997).

Require 2-3 mL of serum for all tests. Draw 4-5 mL of blood (about one teaspoonful) into a red top tube. Spin tube to make clear fluid called serum. Collect serum into a new tube, place cap or stopper, and put some masking tape to secure the cap (this is very important). Then the tube should be wrapped in some padded material like the bubble wrap, and packaged into a shipping box. The package should be sent Monday through Thursday by OVERNIGHT DELIVERY (FedEx/UPS is your choice) to avoid weekend delivery. If it takes more than 24-30 hours for delivery, please include some dry ice in the shipment.

It is absolutely essential that you contact Dr. Singh before scheduling a blood draw or sending a sample.
Dr. Vijendra Singh, PhD
Biotechnology Center
Utah State University
4700 Old Main Hill
Logan, UT 84322-4700, USA
Phone: (435) 797-7193
Fax: (435) 797-2766
Email: singhvk@cc.usu.edu

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I am a member of the anesthesiology faculty at Stanford University Hospital, writing in response to the question of autistic children requiring anesthesia for dental procedures.

There are no data that any anesthetic drug(s) cause or worsen autism, nor are there any published data on preferred drugs for anesthetizing autistic children.

Dental anesthesia is usually performed in the dentist's office. The mandatory requirements are:

1. that an M.D. (or sometimes a D.D.S.) anesthesiologist experienced in dental and in pediatric anesthesia does the anesthesia care, and
   
   
2. that standard hospital operating room monitoring instruments (e.g., pulse oximetry, ECG, and blood pressure), and resuscitation equipment (including a defibrillator) are present in the dental suite.

If the child has serious medical problems (e.g., heart problems, breathing problems, seizures, or airway problems) it is sometimes unsafe to give anesthesia care in the dental office, and the dentist will need to do the procedure in a hospital room setting. This decision is made by the anesthesiologist.

Our standard of care is to make a preoperative phone call to the parent(s), both to obtain information on the child's medical history, and also to describe the anesthetic planned for the child.

The preferred technique for dental office anesthesia is 'deep sedation,' where the child is asleep, without awareness of pain, is breathing spontaneously, and has stable vital signs. The anesthesiologist is in constant attendance.

The anesthetic begins by sedating the child so that an intravenous (IV) can be inserted.

There are two common ways to do this:

1. If the child is cooperative, oral midazolam (Versed), a Valium-like sedative, is given. The child will become relaxed, sleepy, and will separate from the parents with minimal distress. The IV is then started in the operating suite, using a small amount of local anesthetic injected into the skin.
   
   
2. If the child is emotionally uncooperative, an injection is given into the muscle of the shoulder or thigh. We use a combination of midazolam, ketamine, and atropine. This combination reliably produces a sleeping child in 5 - 10 minutes. At this point, the child is separated from his parents, and the IV is started in the operating suite.

The monitors of vital signs are applied to the child, including the pulse oximeter, the electrocardiogram, the blood pressure cuff, and a stethoscope. Additional sedation is added via the IV as needed to maintain the deep sedation state safely. Typically we add narcotic pain relievers such as meperidine (Demerol), or the short acting sedative propofol. Local anesthetic is sometimes injected by the dentist.

When the dental procedure is finished, the child stays at the facility until safely aware. This usually requires a minimum of 30 minutes.

Post-anesthesia side effects are sleepiness, sometimes nausea, and in some children, aggressive behavior or agitation.

When dental sedation is done by an experienced anesthesiologist with modern monitoring equipment and medications, the rate of major complications should be low. The risk of driving in the car to the dental office should exceed the anesthetic risk.

Please refer to our anesthesia website at www.aamgpaloalto.com, particularly the sections on dental anesthesia and pediatric anesthesia. Email response is provided.

Richard John Novak, M.D.
Clinical Associate Professor
Stanford Department of Anesthesiology

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1. Immunosciences Laboratory
   A diagnostic and research facility that specializes in innovative microbiology and immunology laboratory testing. Provides neuro-immune autism panels, including the "McCandless" panel. http://www.immuno-sci-lab.com/index2.html
2. Metametrix Clinical Laboratory
   Provides ION, amino acids, organic acids and other tests. http://www.metametrix.com
3. Great Plains Laboratory
   Diagnostic and sensitivity testing for autism, ADHD, bowel disorders, candida, celiac, chronic fatigue, food allergies and intolerances, immune system dysfunctions, heavy metal toxicity, schizophrenia, yeast, and other conditions. http://www.greatplainslaboratory.com/
4. Doctor's Data
   Provides data on levels of toxic and essential elements in hair, and elements, amino acids, and metabolites in blood and urine. http://www.doctorsdata.com/
5. Great Smokies Diagnostic Laboratory
   Lab known for their Comprehensive Digestive Stool Analysis (CDSA), plus many other tests. http://www.gsdl.com/
6. Pfeiffer Treatment Center
   A non-profit medical research and treatment facility in Naperville, Illinois specializing in research and treatment of biochemical imbalances. http://www.hriptc.org/

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by Teresa Binstock June 1, 1999

Introduction

In recent years, biological aspects of autism-spectrum disorders are becoming documented, researched, and treated. Much of the credit goes to Bernie Rimland and the DAN! docs, as well as to pioneers such as Paul Shattock, Andy Wakefield, Bill Shaw, and the persevering folks at the Great Smokies lab -- and to the parents and interested physicians who ordered lab-tests and who continually conduct their own research, whether "at home", via PubMed and the Internet, or via wading into whole-text articles or, in some cases, actually launching clinical studies (1) .

As I survey the growing amount of biological data about autism-spectrum kids, several categories of biological information are apparent. Generally speaking, the new data arise from six primary categories of information; there is some overlap among the categories; and, for most kids whose lab-test data are available, one major category is missing. Here is a general way to refer to the 6 categories of data already established for autism-spectrum kids:

A. Great Smokies lab data
B. Great Plains lab data
C. IAG data (2)
D. Metabolic analysis, hospital traditional E. Blood work-up, hospital traditional
F. Neurologist work-ups, CAT, MRI, EEG, etc


What is missing from the above is a *thorough* immune panel akin to what Hugh Fudenberg, MD, would order, thus making an additional category:
G. *thorough* immune panels

Immunity and infections

I believe that biological aspects of autism-spectrum disorders will not have a firm foundation until thorough immune-panels become part of the overall autism-spectrum database (3). Furthermore, for each specific child, the thorough immune panel may enhance the parents' and physician's understanding of etiologically significant factors for that specific child; and this knowledge ought augment avoiding treatments that may be harmful while aiding in the design of positive treatments for that child.

At the Orlando conference (4), the importance of immune and infectious contributions was conveyed most clearly by Dr. Luigina Romani, who focused upon immune- and infection-related factors that can shift immunity and thereby contribute to persistent or recurring Candida -- an infection that not only is worthy of treating but also is a symptom of the underlying immune shift whose symptoms, signs, and causes need be addressed. Her lecture complemented my own interest and early findings in immunological and infectious profiles of autism-spectrum children.

In recent years a parents of autism-spectrum kids have been sending me the child's immune-panel, often accompanied by other lab reports, occasionally including an entire medical history. As previously mentioned, the most thorough immune panels were ordered by Hugh Fudenberg, MD (5); and most of these reports demonstrate at least one, often two, and occasionally three signs of atypical chronic infection and/or immune atypicality. Importantly, these infectious and immunological signs cannot be identified and delineated by data-sets A thru F in the above list. Instead, to fully comprehend the biological aspects of many (probably most, I'd now say) autism-spectrum kids, immune-panel data are necessary.

Why obtain data about immunity and infections

Rationale

(i) My readings of thorough immune panels of autism-spectrum have revealed that most such lab reports indicate one or several infectious and/or immune atypicalities.

(ii) Consistent with my research the last several years, VK Singh, PhD, and Andy Wakefield, MD, now talk about the viral lesions that accompanied or preceeded subsequent problems -- whether vaccination-induced neuropathies or post-infection autoimmunity (1). Importantly, just as Reed P. Warren, Alma Maciulis, and Roger Burger documented specific, mild genetic mutations in a percentage of autism-spectrum kids, so too has recent research shown that impaired immunity can be induced by chronic infections (6).

(iii) The one set of genes positively associated with a large number of autism-spectrum kids involves null alleles of Complement 4b along with, in many null-C4b-allele individuals, an extended immune-weakening genomic DNA segment (extended haplotype); These findings implicate infectious processes as etiologically significant in many cases of autism, whether in the mother and/or in the fetus, neonate, infant, or toddler.

(iv) Certain of these viruses live forever within humans, but most of us do not create the atypical antibodies levels seen in the autism-spectrum charts I've perused. In other words, not only does the child have the ongoing presence of a given virus or several, but he or she is having a chronic problem with how his or her body is responding to that virus. Furthemore, when this occurs, the child may well have other immune dysregulations as well -- which is also apparent in a goodly proportion of the thorough immune panels I've perused.

(v) Dr. Romani's data point in a similar direction, ie, a person with persistent Candida infections is likely to have an immune shift in a Th2 direction -- which is what some pathogens can do. Furthermore, whereas persistent Candida is important, it is the tip of the iceberg, and represents the fact that an immune-system altered in a Th2 direction is likely (6- 7). However, categories A thru F do not provide data for unraveling this mystery in a specific child. Only Category G tests -- a thorough immune panel -- provide that data.

(vi) Regressions within the autism-spectrum suggest that the neurological basis of the child's traits is not hardwired and is being affected by internal changes. One possibility is that, in *some* cases a viral re-activation from latency is the culprit; and again, categories A thru F are not very helpful in determining the likelihood of chronic, atypical infections and underlying immune shifts (8).

[Here it is important to note that Bill Shaw's Great Plains lab is now offering a number of immune-related tests, and immune tests not offered by Bill and crew can be obtained by other labs (9)]

Overview

Because *most* of the thorough immune panels I've perused contain obvious atypicalities (10a), and because the work of Reed Warren, Roger Burger and others implicates infectious etiologies and immune aspects as significant, I believe that, for many autism-spectrum children (10b-10i), a thorough list of initial immune-panel tests is needed.

What immune tests?

Parents occasionally query the autism-list and other lists asking "What immune tests?" My suggested answer to that question emerges as follows: in a high percentage of kids representing the still small number of immune panels I've perused, *nearly *every *child has signs of a percolating infection or several, far beyond reference ranges. The words underlying, chronic, and atypical are appropriate. In several cases these elevations are accompanied by an obvious immune impairment, eg, no response to a common antigen such as tetanus, mumps, or varicella. That these atypicalities occur suggests that information from a thorough immune panel is extremely important for many and perhaps most autism- spectrum children and would augment their treatment protocols if and as significant data are obtained.

In the context of credit due Hugh Fudenberg, Reed Warren, and VK Singh, an immune-panel my research shows to be significant is presented below.

Initial and long-term use

By presenting a comprehensive list of immune-panel tests, parents and cooperative docs can have a useful starting point for evaluating an autism-spectrum child. Later, if and as biological treatments are enacted, the initial test data will provide a baseline measure for evaluating subsequent therapies.

Resolving an irony

That biological analyses of autism-spectrum kids usually have not included Fudenberg-like immune panels is ironic, given that the Reed Warren et al findings about immune-impairments in autism-spectrum children have been known for so long.

In other words, if these kids have acquired and/or genetic immune- impairments, let's evaluate their viral load and their immune function -- along with the Category A thru F measures already pioneered; and I can't help but think that, in some and perhaps many autism-spectrum kids, the atypicalities measured by Great Smokies, Great Plains, and other labs may well be due to some of the same viral critters and immune-shifts I'm noticing in the Fudenberg-like panels I've seen thus far.

My concern about steroids such as Prednisone

Many autism-spectrum and/or LKS kids are prescribed steroids such as Prednisone, which many parents describe as "it really helped, for a while" and/or "my child's deterioration occurred while on Prednisone".

Importantly, Prednisone is known to be an immune suppressant. Based upon what I've seen in the through immune panels I've perused, I no longer know how a neurologist or other doctor can dare to prescribe Prednisone without first ordering an extensive immune/infectious workup that would indicate whether or not any infectious and/or immune atypicalities are present, especially given the increasingly documented link between certain pathogens and seizures. For instance, Herpes simplex virus (HSV) is now implicated in a goodly percentage of seizure disorders (eg, 11-13); and Predisone's immunosuppressive effects are well known (14).

Bottom line

My opinion as a non-MD researcher is that, for autism-spectrum kid, category G hereinabove -- the thorough immune panel -- needs be obtained by parents and docs. Will the thorough immune panel offer clues for every child? Probably not, but the only way to determine that is to obtain and evaluate the results of the data.

Immune panel data augment findings from the other categories of lab data, and vice versa. Without the thorough immune panel, the pilot is flying with a high degree of blindness.

A Basic Immune Panel for Autism Diagnostics

Review of initial findings

In most *thorough* immune-panel reports that I've perused on behalf of parents of autism-spectrum kids (n<15), tests in the Basic Panel have revealed atypical elevations of EBV, CMV, and/or HHV6; co-occurring infections are common; and other immune atypicalities are seen in some of the panels, including -- even in this small initial sampling and with much variation from child to child:

(a) atypically high elevations of vaccinal antigens or measles,
(b) mild elevations that may reflect adjuvant effects from other antigens or pathogens such as EBV,
(c) non-detected antibodies against a vaccinal antigen (eg, tetanus, varicella, mumps),
(d) increased or decreased numbers of Natural Killer cells,
(e) impaired NK function,
(f) atypical elevations of certain cytokines,
(g) altered ratios of T cell subsets, and
(h) occasional skewing of the child's immunoglobulin levels.

Cavaet

If a parent purchases a thorough immune evaluation, he or she is not guaranteed that meaningful results will come forth. There is no way of knowing what the tests will show, although the child's and the family's medical history can provide clues as to what tests ought not be omitted. For some parents, the money invested in the tests will have been wasted. Furthermore, the data from such an immune panel may place the child and the parents at the forefront of medical research and treatment, which means that data and observations from recent research will have to be utilized (5, 12a-12b).

The Basic Immune-Panel

At one prominent lab, tests constituting what I think of as the "Basic Panel" would cost slightly less than $1500.

The following list sets forth a minimum of tests I believe necessary for an initial evaluation of the child's immunity. There is an emphasis upon herpes class viruses because

(i) they are ubiquitous,
(ii) they impair immunity, and
(iii) most panels I've perused on behalf of autism-spectrum children report atypical elevations of antibodies against one or several of these viruses.

A viral screen is important, especially for IgG antibodies, which would indicate an atypical chronic infection. EBV provides an exception, because it has a variety of proteins that, if reactivated, can generate IgM antibodies; thus for EBV, both IgM and IgG are suggested. Also, if the child has recently experienced a regression, then adding IgM antibodies might be instructive in some cases.

	IgG	HSV1, HSV2, varicella, CMV, HHV6
IgM and	IgG	for an EBV screen
	IgG	measles
	IgG	rubella
	IgG	rubeola
	IgG	coxsackie
	IgG	vaccinal antigens, eg, diptheria, tetanus, mumps
	IgG	for Myelin Basic Protein (16)

The TRH measurement is not traditional but appears to be a very important measurement in autism-spectrum kids.

The following is offered as a set of tests and mimics much of the data presented in the charts I've evaluated:

Tests which are not antigen-specific:

Total T, B lymphocytes
T4/T8 Helper Suppressor Ratio
Activated T Cells
NK count
NK activity
Lymphocyte Immune Function Test (T and B)

In addition to the basic panel

The tests listed above provide an excellent overview of many aspects of the child's immunity. However, pathogen-specific assays are *specific*, ie, they don't provide information about other pathogens. However, the last six tests listed above provide an overview that can reflect pathogens not studied in the pathogen-specific tests.

Nice additions, as appropriate ($750 or less, total)

microflora panel
parasites panel
fungal panel
monocyte/macrophage function
IgG anti-serotonin antibodies
IgG anti-dopamine antibodies

More nice additions

DR CD38 CD45 CDRO
cytokines
IgG subclasses
T-helper 1,2 function
papilloma (PCR of warts)

Case history particulars might suggest from among:

anti-cardiolipin IgM, IgA, IgG
IgE analyses
food panel

In closing

The work of numerous researchers, augmented and expanded by the immunity and infection lab-tests ordered by a few physicians, demonstrate that immune- impairments (whether acquired and/or genetic) appear to play a causal and (in some cases) an ongoing role in a goodly subset of autism-spectrum children. The information from a thorough immune panel is an important contribution to a child's diagnostic profile and treatment options.

References

e-mail to: Teresa Binstock
copyright 1999

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Parents often ask the Autism Research Institute for any available information on anesthesia when their autistic child needs a surgical or dental procedure. In response, we published a request for input from anesthesiologists in a recent Autism Research Review International newsletter. We are delighted to be able to post this excellent article from anesthesiologist, Louise Kirz, M.D. who has two autistic sons. Bernard Rimland, Ph.D.

Letter to my fellow parents:

Dear parents,

Your child needs a surgical procedure and an anesthetic. This can be a frightening experience for any parent and their child. Add to this the special needs of a child with autism and many of us throw up our hands and say, "How in the world am I going to get (us) through this one!" As a parent of two autistic boys I understand what you are going through. There is always one more thing that we need to get our child through. As a board-certified anesthesiologist, I also understand the problems faced by trying to anesthetize one of our special children. Here is a partial list of suggestions and information for parents and anesthesiologists.

1. Schedule a preoperative visit with your child's anesthesiologist if at all possible. Sometimes it may be with an anesthesiologist in the group, but may not be the anesthesiologist who will be taking care of your child. If this is not possible ask that your child's anesthesiologist call you prior to the date of surgery.
2. Read number one again. A preoperative visit or phone call is the single most important thing you can do to ensure a smooth experience for everyone involved. Discussing your child and his or her particular needs, fears, communication level, ability to cooperate and understand with the anesthesiologist will go along way toward easing everyone's anxiety.
3. Listen to the anesthesiologist. There are many acceptable, safe approaches to anesthesia. Anesthesia is not an exact science. I like to compare it to baking a chocolate cake. You can use cake flour, wheat flour or rice flour, (for the GFCF among us). Margarine, butter or oil? Baking chocolate or cocoa? Eggs or egg substitutes? There are many ingredients and many choices. It is best to stick to what the cook (anesthesiologist) thinks is best and is most comfortable with. If your child is taking medications the anesthesiologist will have some very specific directions for which the child should take the day of surgery. Listen very carefully to the instructions about not eating prior to surgery. This is very important. Your child could get a dangerous pneumonia if anesthetized with a tummy full of food.
4. After reading number 1, 2 and 3 remember that if for whatever reason you are not happy with what you hear from your child's anesthesiologist you can request a different one. Feel free to ask the anesthesiologist if he or she is at ease with your child's special needs.
5. Prepare your child as you would for any unusual activity. You know your child the best. If social stories or pictures work for him or her do that. If you think a preoperative visit to the hospital would help, ask for that to be arranged. Read a book, sing a song, do a dance.... whatever will help your child to understand what is going to happen to him. Of course you need to know what exactly will happen too. Be sure to ask for the exact sequence of events. When does he need to put on the hospital gown, will they draw blood, does he get an IV (and when) can he bring a favorite item into the operating room with him. Who will be there when he wakes up? Ask, ask, ask, then call them back and ask the questions you forgot.

Thumb nail sketch of Anesthesia

Anesthesia can be broken down into three basic types: general anesthesia, regional anesthesia and sedation anesthesia. (Otherwise known as MAC anesthesia or monitored anesthesia care.)

1. General anesthesia: What most of us think of when we say anesthesia. This is the big deep sleep during which the patient is totally unaware of his surroundings. This is the type of anesthesia that most of our (and other) children will need to undergo for most surgical procedures.
2. Regional Anesthesia: Spinal anesthesia, epidural anesthesia, and individual nerve blocks. The patient is awake and aware but many are a little sedated. Would be used in our kids only if they were exceptionally cooperative. Very rarely done as the sole anesthetic in children even the typical ones. May be used with general anesthesia to provide additional pain relief after the operation.
3. Sedation anesthesia: Patient is groggy but not totally asleep, as they would be with a general anesthetic. Might be used for minor procedures such as x-rays or CT (CAT) scans. (My child had this kind of anesthesia for a special x-ray procedure on his bladder. I was convinced that he would need a general anesthetic, but I listened to my child's anesthesiologist and went along with his plan instead ... guess what? The anesthesiologist was right, my child did fine with this for this particular procedure.)

I will focus a little more on general anesthesia since most of you will be facing this option. I will discuss the process your child will probably go through, and some of the choices you and your child's anesthesiologist will have