Treatment of Lyme's and AUTISM... Raphael Kellman, M.D.

[Guest guest]

http://raphaelkellmanmd.com/?page_id=361

Health Issues We Treat

Lyme Disease

I’ve treated many patients with Lyme disease over the past 13 years. Most of these people had come to my office complaining of a diversity of lingering symptoms. These include migratory joint pain, fatigue, forgetfulness (sometimes called “brain fogâ€), mood swings, constant headache, and sensory abnormality. When symptoms of Lyme disease persist or recur, it usually indicates that the infection has progressed from an early stage to a later, more entrenched stage. At this point, treatment often requires antibiotics, orally or intravenously, and sometimes in lengthy or repeated courses, I use antibiotics, but I add a variety of natural treatments. These include: TOA Free Cat’s Claw, antioxidants, natural antibiotics, liver detoxifiers, immunological stimulators, hyperbaric oxygen, and probiotics and probiotics. Information about the natural treatments I’ve found helpful in Lyme appears under subheads further along in this

article Lyme disease is difficult to treat in later stages. The Lyme pathogen has several ways of evading antibiotic kill and host immunity. It can invade intracellular sites, has a slow rate of growth, can remain dormant in atypical forms for long periods, and may sequester in areas antibiotics can’t easily penetrate. It’s imperative, then, to combine antibiotics with natural therapies. LYME DISEASE AND LOW THYROID Lyme researchers and clinicians have observed an association between Lyme infection and hypothyroidism (low thyroid). The inci­dence of thy­roid invol­ve­ment in Lyme disease may be grea­ter than expec­ted from the nor­mal popu­la­tion. In many of these patients, the thy­roid dys­func­tion was observed to ori­gi­nate in the pitui­tary or hypothalamus. So it is vital in treating Lyme to test for low thyroid. There are a variety of tests for low thyroid. The one I use,

the TRH Stimulation Test, can definitively show low thyroid in connection with Lyme disease. When the TRH test indicates low thyroid, I treat Lyme patients with natural thyroid hormones. Time and again, I’ve seen that this treatment has significant beneficial effects on numerous symptoms suffered by patients. It helps especially with the fatigue, muscle and joint pain, “brain fog,†and some neuropsychiatric issues. LYME DISEASE; BASIC INFORMATION The manifestations of Lyme disease are protean, suggesting the symptoms of numerous other illnesses. Lyme is such a mimicker of different conditions, it’s been called â€The Second Great Imitator†– the “first†great masquerader being syphilis, caused by a bacterium similar to the Lyme pathogen. For persons interested in what is solidly known about Lyme, the information that follows offers reliable basic information. CAUSE AND TRANSMISSION The Borrelia genus consists of three different

spirochetes (spiral-shaped bacteria). The third, identified in 1982 and named Borrelia burgdorferi (Bb), is responsible for Lyme disease in humans. Female ticks belonging to the Ixodes ricinus complex are the primary vector (carrier) of Bb to humans. The Centers for Disease Control and Prevention (CDC), believes that another tick species, Amblyomma americanum, transmits a spirochete-caused illness closely resembling Lyme in the US Southwest and Midwest. The CDC calls the spirochete involved in this illness Borrelia lonestari and the illness STARI (southern tick-associated rash illness). Ixodes and Amblyomma ticks coexist in many US regions. In their larva, nymph, and adult stages, Ixodes ticks have one blood meal; larvae in late summer, nymphs the next spring and summer, and adults during the fall. Compared with the common dog tick, Ixodes ticks are smaller, their legs black, and the nymph form smaller than a poppy seed. Larvae and nymphs

prefer the white-footed mouse as a host in most of the US. Adults prefer the white-tailed deer. After attachment by a Lyme tick to a human, the time of transmission of Bb ranges from 12 to 72 hours, but there are documented cases where transmission has occurred in less than half a day. Pregnant women may also transmit Bb to fetuses. INCIDENCE Today, new Lyme cases make up 95 percent of the total number of vector-borne diseases reported annually to the CDC. In the past few years, all 50 states have reported Lyme or Lyme-like illnesses. The majority of new case reports have been pouring in from Northeastern, mid-Atlantic, and north-central states. Reports from California, Texas, and Florida are on the rise, indicating that Lyme disease in gaining a foothold in these highly populated states. And the incidence is soaring; over 12,000 nationwide in 1997, almost 17,000 in 1998, close to 24,000 cases in 2002. But the actual incidence of Lyme in the US is

uncertain. According to the CDC, it accepts only ten percent of reports of new Lyme cases. The chief limiting factor is the CDC case definition, utilizing very narrow criteria and developed not for clinical diagnosis but for surveillance alone. So in 2002, for instance, when the CDC reported 24,000 new cases, the true number of new Lyme cases around the country may have totaled 240,000! STAGES Lyme disease may proceed through several stages, affect various organ systems, and persist or recur if not correctly diagnosed and treated early and properly. During the first stage of Lyme, many infected people develop a reddish rash, often roughly circular, at the site of the tick bite. Called erythema migrans (EM), normally the rash expands, clears in the center, and resolves in three or four weeks. Note: the typical EM rash does not appear in a significant number of infected persons. Or it may take an uncharacteristic form, or develop in a part of the body

unlikely to be noticed by a Lyme-infected individual. Estimates on how frequently EM presents uncharacteristically or goes unnoticed or unrecognized range from 20 to 50 percent. Chills, a flu-like illness with fever, mild fatigue, or myalgia can be additional manifestations of Lyme during the first stage of infection. The disseminated stage of Lyme disease begins when the spirochete passes into the blood or lymph. Signs and symptoms of dissemination vary greatly and can occur less than a month after infection or as much as a year or more following a bite by a tick carrying Bb. Whether in early disseminated Lyme (manifesting weeks or months after infection), or late, persistent Lyme (manifesting many months or even years after infection), the illness mostly affects the musculoskeletal system, the central nervous system, or the skin. Between five to ten percent of Lyme patients experience heart problems, which can be acute during the early disseminated

stage. Incorrectly diagnosed and treated, up to 20 percent of patents in the late persistent stage develop neurological disease, which can also be acute In general, Lyme in the persistent stage presents with musculoskeletal or neurological involvement. DIAGNOSIS Diagnosing Lyme disease is a complex, often uncertain process .A large number of multisystem manifestations can cloud the picture, and Lyme signs and symptoms during both the early and late stages can appear like the clinical manifestations of many other conditions… The CDC advises physicians to make a clinical diagnosis if they suspect Lyme disease. There are two bases for such a diagnosis. 1- Identification of the EM rash in an early stage, or involvement of a major system backed by positive serology. 2- Recognition of clinical signs characteristic of Lyme, a history of exposure in a geographic area where Lyme ticks are endemic, and the use of lab tests as an adjunct to diagnosis. Two lab

tests are usually ordered to support a Lyme diagnosis: the ELISA and Western blot. These tests supply indirect evidence of the presence of Bb, measuring the immune system’s response to the spirochete. ELISAs detect antibodies in the patient’s serum that react to antigens (proteins that evoke an immune response) present in the Lyme spirochete. A patient having such antibodies probably has been exposed to Bb. But Lyme ELISAs are notoriously deficient in two ways. They are not sensitive to certain true antibodies of Lyme, and they are over sensitive to antibodies seen in many non-Lyme conditions, periodontal disease, for instance. Western 20blots are used to distinguish between true and false positives on LISAs. The Western blot test looks at antibodies directed against a wide range of Bb proteins. In a patient with antibodies to a particular Bb protein, a “band†forms at a certain place on the blot. “Reading†the “band†patterns formed by

the spectrum of Bb antibodies, labs are able to determine with greater specificity if a patient’s immune response is specific for the Lyme spirochete. Indirect antibody detection has significant limitations. Patients vary considerably in their serologic reactions to Bb. Patients are expected to test negative in early Lyme because of the time required to develop detectable antibody levels. During the early period of disseminated Lyme, patients treated with antibiotics may have negative or equivocal serologies; presumably, the antibiotics nullified their immune response. In other patients, antibodies are detectable long after treatment, which makes it difficult to distinguish between active or past infection. Also, antibodies can form complexes with antigens, but current antibody tests only detect free antibodies. STANDARD TREATMENT FOR LYME DISEASE Many cases of Lyme disease, diagnosed soon after infection, respond to relatively short-term antibiotic

therapy and don’t recur. Diagnosed in a late stage, Lyme is much less responsive to antibiotics. Giving antibiotics orally or by IV in repeated longer courses or for lengthy periods appears to provide relief. NATURAL TREATMENTS FOR LYME DISEASE TOA FREE CAT’S CLAW Cat’s Claw is an herb native to South America. This form of Cat’s Claw has been shown to help control inflammation and microbial balance and sooth irritated tissue in the GI tract. It also appears to have antioxidants which help modulate and support immunity. TOA Cat’s Claw contains as well quinovic and glycosides, both natural precursors to quinolone antibiotics. (Quinolones are a family of synthetic broad-spectrum antibiotics that prevent bacterial DNA from unwinding and duplicating.) GLUTATHIONE, A POWERFUL ANTIOXIDANT Glutathione, given intravenously (IV) and orally, plays a vital role in liver detoxification; glutathione also seems to have a significant effect in neurological

Lyme. LAURICIDIN, A NATURAL ANTIBIOTIC Derived from lauric acid, a fatty acid occurring in laurel, coconut, and palm oils, lauricidin appears to reduce Lyme neuro-toxicity. AHCC, ACTIVATOR OF NATURAL KILLER CELLS AHCC, derived from medicinal mushrooms grown on rice bran, stimulates the production of natural killer cells. Natural killer cells (NK cells) belong to the innate immune system. Their special function in immunity mostly involves targeting and killing cells infected with viruses or host cells that have turned cancerous. HYPERBARIC OXYGEN THERAPY Hyperbaric oxygen increases the production of energy, blood flow, and production of ATP, a molecule essential for cellular energy production. Hyperbaric oxygen also appears to help in neurological Lyme issues. PREBIOTICS AND PROBIOTICS Long-term antibiotics can impair normal gastro-intestinal (GI, or “gutâ€) functioning, I’m hyper-vigilant about monitoring and improving GI function. I give my

patients probiotics and probiotics to maintain function. Probiotics are nutrients that help healthy GI bacteria to grow. In my clinical experience with Lyme, the most effective include inulin, oligofructose, betaglucan, and larcharabinogalactan. Inulins are a group of naturally occurring polysaccharides (several simple sugars linked together ) produced by many types of plants. Oligofructose is a subgroup of inulin. Betaglucan comes from a different group of polysaccharides. And larcharabinogalactan is a species of Echinacea. Betaglucan improves immunity generally. Larcharabinogalactan improves immune response, too. Probiotics replace GI flora (microorganisms) reduced by antibiotics. I give Lyme patients various acidophilus cultures for replacement, but I’ve found saccharomyces boulardi (a tropical strain of yeast) to be more effective as a probiotics in the large and small intestines than the bacteria lactobacillus). S. boulardi

seems particularly effective in auto-immune conditions, and Lyme can have an auto-immune component. Note: In monitoring GI function in Lyme patients, I’ve learned that it’s frequently necessary to test stools for overgrowth of certain gut bacteria. OLIVE LEAF EXTRACT This is a natural compound with apparent anti-Lyme activity. Clinical evidence shows that carefully produced extracts of olive leaf lower blood pressure. Bioassays at the lab level suggest that olive leaf extracts have antibacterial, antifungal, and anti-inflammatory effects. Recently, a liquid extract from olive leaves was shown to have an antioxidant capacity twice that of green tea extracts and an antioxidant capacity 400% higher than Vitamin C. LYME RESEARCH; LATEST FINDINGS As the 21st century heads into its second decade, controversies and questions about Lyme disease still await resolution. Among them: Historically, Lyme emerged as a separate disease entity in the US

from the mid-1970s to the early 1980s. A cluster of cases of children with severe arthritis in Lyme, CT, studied and reported by academic physicians associated with Yale University, is commonly taken as the starting point. Some 35 years later, every state in the Union has reported Lyme cases to the CDC, and with the true number of new cases most probably underreported annually, this tick-borne infection may have reached epidemic status. How does one account for the dramatic, rapid spread? It’s been recognized almost from the onset that the Lyme spirochete has a number of different strains. How many? Are the strains alike or dissimilar in their ways of affecting people? If Lyme infection can persist, as some clinicians and many patients say, how does the spirochete avoid detection and elimination by the host’s immune system? Studies have indicated that antibiotics don’t eradicate infection in later stages in all cases? How do Lyme bacteria

“hide†from antibiotics? Why does Lyme disease vary so greatly from patient to patient? Pamela Weintraub, senior editor at Discover magazine, who’s covered medicine and science in the national media for 25 years, recently published a book about Lyme disease. Titled CURE UNKNOWN: Inside the Lyme Epidemic (St. ’s Press, NY, 2008), Weintraub’s book features recent research findings that are outdating 20th-century theories about the nature and treatment of Lyme. Studies of the Lyme spirochete’s genome and the proteins created to protect the spirochete are the “hot†fields in 21st-century Lyme science; these fields hold the greatest promise for improving diagnosis and treatment. I keep current on reports about Lyme disease in the medical literature. For people with little professional reason to read this literature, CURE UNKNOWN surveys most of the important findings, particularly on persistent or chronic Lyme. STUDIES BY

LUFT-SCHUTZER On the apparent outbreak of Lyme in the US in the mid-1970s, Weintraub discusses one persuasive theory with Ben Luft, an infectious disease specialist at Stony Brook, Long Island. One of the big discoveries from research on the genome of the Lyme spirochete, she explains, is that the dominant strain, B31, is identical genetically in the US and in Europe, suggesting a transcontinental migration of the organism in recent years. Luft comments: “If the organisms had been separated longer, they would be different, because each would have been evolving in its own way.†Weintraub continues: “The data suggest that sometime before the epidemic took off, a strain from Europe may have arrived in the US on the back of a dog or a bird, lighting the forested suburbs like a match thrown on tinder wood.†She concludes: “But it wasn’t B31 alone that fanned the flames. In any given region, there could be a different mix of strains. The farther

investigators traveled from the Northeast, the more variable and mixed the strains became, implying that the disease could produce different symptoms from person to person and different results from Lyme test to Lyme test.†Luft’s investigative team looked at 20 strains of the Lyme spirochete isolated from ticks collected from New Hampshire to the Carolinas, comparing differences in their genes. The investigators determined that six strains don’t infect humans. Ten cause only a rash. But four strains can get past skin and invade other tissue. B31 proved the most virulent of these four. Recently, Luft’s team joined with Schutzer, an immunologist at the University of Medicine and Dentistry, NJ, to see what causes B31 and the three other invasive strains different. The Luft-Schutzer teams discovered that the invasive Lyme strains can exchange genetic material with each other. (The non-invasive strains “reproduce†by cloning.)

Luft-Schutzer is now designing studies that will sequence every gene in every strain of the Lyme spirochete from the Northeast, and genes in strains from the Midwest and Europe. Through recombinant biology, the team will get each gene to express its individual protein in the lab. The number of individual genes expressed could total 1,800 proteins altogether – every protein expressed by every protein. Then, instead of testing patients for antibodies to the very limited number of proteins that the CDC has called for since the late 1990s, Luft-Schutzer will coat all 1,800 Lyme proteins on a slide, making it possible to test patient sera against the whole spectrum of Lyme proteins in their entire variability. STUDIES BY BARTHOLD AND NORRIS Weintraub’s chapter “Secrets of an Evil Genius: The Evidence for Persistence,†centers on animal research by Barthold, a veterinarian involved in gaining insights into the survival

mechanisms of the Lyme spirochete, first at Yale back in the early 1980s, lately at the University of California, . Barthold’s observations through his Yale years showed that the Lyme spirochete could persist in mice and other mammals even after aggressive antibiotic treatment. “You have a bacterium,†Barthold tells Weintraub, “with a relatively small and simple genome that can do incredibly complex things. It is a fascinating organism with a lot of evolutionary intelligence, consistently capable of creating persistent infection and evading host immunity.†Barthold published a paper in Antimicrobial Agents and Chemotherapy in 2008 on a controlled investigation in mice. One arm followed mice given ceftriaxone after three weeks of infection (early acute disease). A second arm followed mice treated with the same antibiotic after infection for four months (late, persistent disease). Paralleling the treatment arms, there was a control arm of

mice on saline solution. All the mice were sacrificed to search for persistent infection, Weintraub reports that “Barthold found that after he treated acute or chronically infected mice with high-dose antibiotics, he achieved cure by virtually every ordinary measure, from clinical signs of disease to growth in culture. Yet three months later, small numbers of spirochetes remained, hunkered down in the collagen of the heart and joints. Moreover, in the chronic mice, these spirochetes remained infectious; they could be picked up by ticks and transmitted to other mice as active infections.†Weintraub notes a key new finding in Barthold’s paper. The treated spirochetes were attenuated in their ability to replicate. This finding, she remarks, opens “a window on the experience of human patients with chronic infection…If spirochetes responsible for persistent disease can’t replicate, antibiotics that kill bacteria by hitting bacterial cells as they

divide may not work. “And as long as these ‘attenuated’ spirochetes stay alive, they may not aggregate in a mass critical enough to cause the gross inflammatory signs of Lyme arthritis or meningitis. But they could cause the ‘constitutional’ symptoms suffered by chronic patients. Researchers term these symptoms ‘pro-inflammatory effects,’ and they include production of nitric oxide and the activation of neutrophils and macrophages, which together could account for the fatigue and malaise so many of these patients report.†Turning next in this chapter on the evidence for persistence of Lyme to research by Norris, a microbiologist at the University of Texas, Weintraub describes a discovery Norris made in the late 1990s, which he published in the journal Cell. In experiments with animals, Norris found a special DNA segment that creates new gene sequences. These new genes produce new Lyme spirochete proteins. As the proteins

change, the spirochete coat also changes, and molecules spewed out by the host’s immune system to kill the Lyme spirochete lose their killing power. Through ‘promiscuous recombination’ of the genes, a “vast array of proteins†(Norris’ language) swiftly generates into a system so extensive, it can “potentially create millions of antigenic variants in the mammalian host†(Norris’s language again, emphasis added). In a follow up on this discovery, Norris reported in 2008 that this novel mechanism responds to cues in the environment, facilitating the Lyme spirochete’s survival “from locale to locale†(Weintraub’s words here). The process can also be “dialed up or down†(Weintraub’s language again) through fluctuations in the temperature and acid content of surrounding tissues and cells. STUDIES BY WEIS Janis Weis, an immunologist at the University of Utah, has studied why Lyme disease varies from individual to

individual. Working with mouse tissue cultured in vitro, she exposed it to the Lyme pathogen and observed that while B and T cells generated by the immune system destroyed spirochetes, a more generalized inflammatory response, occurring before B and T cells appear, damaged the mice. Investigating further, Weis discovered a molecule, termed “Toll-like receptor 2,†which initiates the inflammatory reaction. Mice that lack this molecule develop little inflammation. Over time, the load of spirochetes grows huge, until these mice show inflammation more disabling than that in mice with more pro-inflammatory genes, Noticing that some mice got much sicker than others, even when exposure to Lyme was exactly the same, Weis asked: Were some mice (and some people) simply less susceptible to inflammation? To answer her question, she crossed severely and mildly arthritic mice over generations, so all kinds if intermediate combinations emerged.

After years of interbreeding, she created 400 mouse lines, each line at a different point on the spectrum – from those prone to severe inflammation to those incapable of any inflammation. Infecting all 400 lines with Lyme, she found a full range of disease severity, which corresponded with the genetic background of the mouse. Depending on where mice fell on the spectrum, even a small number of spirochetes could induce and sustain their genetically predetermined variety of disease, No matter where on the spectrum an individual fell, when all the Lyme spirochetes were eliminated, the signs of the disease disappeared. So where an individual falls on the spectrum may not make a difference – unless that individual gets Lyme. The same system exists in humans, Weis believes, and probably accounts for why different people have such different disease outcomes. CLOSING NOTE In sharing this information on the latest research on Lyme disease, I chose findings

on persistence of infection and variability in symptoms and outcomes because these areas are among the most debated issues and least resolved questions in Lyme. Bear in mind while reading this information that until these issues and questions are resolved, many people will continue to become infected with Lyme yet fail to receive early diagnosis and treatment. And late stage Lyme, experts estimate, is incurable in 20% of adults!

AUTISM: TESTS AND TREATMENTS I USE

My treatment program has helped hundreds of autistic children. It can also help your child. To make an appointment, call .

My understanding of autism is rooted in systems theory, the theory that scientists use to explain the natural world. According to this theory, systems work together in nature and in the human body to produce the whole, and the whole is more than the sum of its parts. The new diseases of childhood, like autism, result from a poor and delayed development of this integration. My success in helping so many children with autism and ASD rests in my restoration of this integration. This requires not only knowing how to practice the science of medicine but also the art of medicine.

Information on the tests and treatments I do follows.

NOTE: This is a general outline, which needs to be individualized with each patient.

Autism begins in early childhood. It is mainly characterized by dysfunction in the immunological, gastrointestinal, endocrine, and neurological systems, and is much more likely to appear in boys than in girls. (Research has not yet disclosed why.) In healthy children, these systems work in a coordinated, integrated fashion. Children with autism lack this integration.

More and more studies are revealing the complex web of biological and environmental causes that underlies autism. As an internist and a holistic medical doctor for the past 15 years, steeped in the philosophy of medicine and science, I’ve woven together the strands of research on how autism develops, how the affected systems interrelate, and, most important, how to combine and sequence holistic treatments that quickly improve autistic children.

My most important contribution to this field is that hypothyroidism (low thyroid) has neared epidemic proportions in children with Autism Spectrum Disorder (ASD). Routine tests for hypothyroidism in autistic children, including the TSH test, frequently fail to detect low thyroid. I’m detecting this epidemic because I use a more sensitive thyroid test, the TRH stimulation test. Doctors relying on routine tests, even those who treat autism, frequently miss hypothyroidism in ASD patients for years.

The Center for Disease Control and Prevention (CDC) offers a plausible explanation for the prevalence of low thyroid in so many autistic children. Perchlorate, one of many chemicals that developing children are exposed to, has been seeping into our drinking water and food crops. This chemical can adversely affects human health by interfering with iodine uptake into the thyroid gland. In children, the thyroid helps in proper brain development, and increased exposure to perchlorate may impair normal development in individuals prone to ASD.

Additionally, scientists have recently found that polychlorinated biphenals (PCBs), built up in our environment, not only cause brain dysfunction but also thyroid dysfunction. Production of PCBs was banned by the United States Congress in 1979 because of their toxicity and classification as a persistent organic pollutant. Concerns about the toxicity of PCBs are largely based on compounds which share a structural similarity and toxic mode of action with dioxins (polychlorinated dibenzodioxins, a group of organic compounds that have been shown to bio-accumulate in humans and wildlife and are known mutagens and suspected human carcinogens).

Based on the TRH stimulation test, I’ve been treating autistic children with natural thyroid hormone. I’ve found that hyperactive children became calm – sometimes, within a week. Some became more verbal. Within one to three months, over 90% of my autistic patients have experienced extraordinary improvement, and a smaller percentage a remarkable recovery. Attention span, cognitive function, language, and sociability have improved significantly in these children. (The use of thyroid hormone also helps other treatments work much better.)

I’ve found no other treatment for autism is as effective as thyroid hormone. If physicians miss hypothyroidism in autistic children, then one of the most significant factors in the etiology of their disorder will be left untreated and their brain will not be able to develop normally.

TESTS I MAY DO AFTER AUTISM IS DIAGNOSED

Most autistic children who come to me for treatment have had a confirming diagnosis. But a diagnosis by itself does not adequately detail the particular web of biological and environmental factors that is causing autism in an individual child. To begin to unravel this web for each child, I may order certain tests. The basic tests include:

Thyroid hormone levels. Hypothyroidism (low thyroid) can have a profoundly deleterious effect on the developing brain, significantly contributing to the development of autism. The routine thyroid blood tests (TSH, T4, and T3) are unreliable for detecting low thyroid.

The most sensitive thyroid test, called the TRH stimulation test (once the standard thyroid test, and the one I’ve used to discover the thyroid-autism connection), uses a hormone called TRH to stimulate the pituitary gland into releasing a hormone called TSH. If TSH is very high upon stimulation, the thyroid is low. (Read my article on the thyroid-autism connection).

Complete blood count (CBC). A CBC looks at the various kinds of blood cells for abnormal findings that relate to autism.

Complete metabolic panel (CMP). A CMP looks at the levels of electrolytes, minerals, and proteins to spot blood sugar problems, dehydration, kidney or liver disease, or malnutrition in general.

Amino acids. Levels of amino acids secreted in urine can provide important clues about contributory factors in autism. These acids are the biochemical building blocks of neurotransmitters that act on the brain to influence mood and behavior. The proper balance of these nutrients in children is necessary for healthy emotional and cognitive development. Deficiencies of essential and semi-essential amino acids, especially the sulfur amino acids methionine, cystine, and taurine, may also indicate chronic digestive dysfunction. This can lead to dysbiosis (imbalanced microbial flora in the gastrointestinal tract.).

Essential fatty acids (EFAs). EFAs, which can’t be made by the body, are required for many crucial biochemical processes. There are two groups: omega 3 and omega 6. The relative levels of these groups are critical to the development and health of the brain and the body. If the level of omega 6 is much higher than the level of omega 3 in the diet, there can be negative effects on behavior, cognition, and mood.

Organic acids. These are metabolic intermediates produced in pathways of central energy production, detoxification, intestinal microbial activity, and neurotransmitter breakdown. Accumulation of specific organic acids in urine often signals a metabolic inhibition or block, possibly due to a drug effect, an inherited enzyme deficit, nutrient deficiency, or toxic build-up. Testing for organic acids can reveal activity and changes at the metabolic level, helping practitioners discover hidden issues and pinpoint where therapeutic focus is needed.

Stool analysis. I do this test mainly to detect dysbiosis, a condition where there are abnormal bacterial, viral, or yeast populations in the intestines. The nature and severity vary from child to child. In autism, we need to find out if anaerobic bacteria – particularly bacteroides and clostridium – and yeasts such as candida are over-flourishing. The effect on brain function of two such peptides, Casomorphin and Gluteomorphin, have an effect on brain performance similar to that of morphine.

Casomorphin and Gluteomorphin in blood are produced by the bacteria from incompletely-digested casein and gluten (contained in milk and wheat products respectively). With autistic children unable to tolerate casein and/ or gluten, the levels of Casomorphin and Gluteomorphin in the blood and tissues can be high enough to cause an area of the brain known as the Amygdaloid body to stop functioning normally. This dysfunction affects nerve pathways which control learning and communication.

Some 80% of autistic children have some degree of dysbiosis - either constipation or loose, foul-smelling stools - and it is very important to detect and correct this.

Heavy metals. The most serious forms of environmental toxins that children are exposed to are heavy metals. Mercury and lead top the list, followed by aluminum, arsenic, and uranium. Several tests will measure heavy metal exposure.

Researchers have found very low levels of toxic metals in hair samples of infants later diagnosed with autism, suggesting that these children have defective detoxification mechanisms, which causes heavy metals to remain in their bodies. Eventually, the buildup of heavy metals results in digestive and neurological abnormalities.

Herpes Viruses 1, 2, and 6. These forms of Herpes can cause low grade intestinal inflammation in autistic patients. Some investigators believe there is an autism-spectrum subgroup wherein the infant or child’s gastrointestinal pathology provides the route by which herpes simplex virus migrates into the central nervous system to produce autistic symptoms.

Epstein Barr. This virus may cause chronic abdominal pain in children with autism.

I may also order a liver function test, (footnote 1) a vitamin and essential nutrient blood test, (footnote 2) a full evaluation for Lyme disease and co-infections, an IGG food allergy test, (footnote 3) and a porphyrin test. (footnote 4)

MY THREE-TIER (OR THREE LEVEL) TREATMENT FOR AUTISM

Over the many years that I’ve been treating autistic children, I’ve followed a three-tier (or three-level) approach to treatment. This approach produces the quickest, most effective results.

Note: It is vital to understand that treatments have to be given in correct sequence, which may vary from child to child. How these treatments may be given over time also varies from patient to patient.

Note well: These treatments must be administered by a physician extremely experienced in autism and these therapeutic compounds.

First Tier.

Dietary changes. I always start with dietary changes, recommending the avoidance or removal of foods likely to induce various aspects of autism.

Exclusionary diets. I also start autistic children on diets that exclude foods and components of foods known to trigger autistic behavior – casein and gluten, to cite common triggering components.

Low thyroid. Since low thyroid is a crucial factor in ASD, once I detect hypothyroidism through the TRH stimulation test, I immediately introduce corrective treatment with thyroid hormone.

Second Tier.

At this level, nutritional supplements and natural compounds that improve metabolic function provide major benefits. Metabolic dysfunction is a characteristic of autism, which can lead to toxicity in the brain and also hypothyroidism.

Bear in mind that autism is a multifaceted disorder, with direct damage to the immune, gastrointestinal, nervous, and endocrine systems. After damage, these systems begin to injure one another in a vicious spiral of interwoven injuries. Consequently, autistic children may suffer mitochondrial damage and dysfunction, inflammation of the brain and gut, severe nutritional deficiencies, food reactions which have neurological ramifications, autoimmune attacks, and immune system over-activity and under-activity. Eventually, all this can lead to hormone deficiency, gastrointestinal dysfunction, and brain dysfunction.

The treatments I give in this second tier aim primarily at detoxification, correction of hormonal deficiencies, restoration of brain function, neurological-enhancement, and immunological modulation.

Here are elements, supplements, vitamins, and other natural substances appropriate for my second tier of treatment for autism:

Taurine. Levels for taurine, an amino acid, are low in many autistic children. Taurine helps cells detoxify and also helps prevent seizures.

Glutathione. A tri-peptide consisting of three amino acids -glycine, cysteine and glutamic acid. Glutathione is an anti-oxidant that helps protect the nervous system. In the liver, glutathione plays a crucial role in detoxification.

Methylcobalamin. The active co-enzyme form of Vitamin B12, Methylcobalamin is the only type present in the brain. It is required for transporting the vitally important methyl groups which activate neuro-transmitters and improve brain function. Methylcobalamin is crucial for the methylation pathway, which often is dysfunctional in autism and ASD. Methylcobalamin is essential for successful treatment of autism and ASD. It must be given by injection. There is no known toxicity.

Probiotics. Administered in adequate amounts, probiotics are live microorganisms which confer a health benefit. Lactic acid bacteria (LAB) and bifidobacteria are the most common types of “friendly†microbes used as probiotics. Probiotics are commonly consumed as part of fermented foods with specially added active live cultures (such as in yogurt, and soy yogurt), or as dietary supplements. Autistic children are frequently deficient in probiotics, so probiotic supplementation improve gastrointestinal and immunological function

Saccharomycin Boulardi. Lactose and dairy free, this probiotic maintains healthy gut ecology, serves as an anti-toxin against harmful diarrhea causing pathogens, and supports healthy intestinal mucosal lining. It also modulates and improves immunological function. (See part 2 of this article for further discussion of the need and benefits of probiotics.)

Peridoxal 5 phosphate. This is the active form of Vitamin B6, an essential vitamin that is necessary for more than 60 biological processes in a healthy human body. The body converts Vitamin B6 into pyroxidal-5-phosphate (P5P), a compound that is used to release energy from carbohydrates and starches, and to break down proteins. P5P is also used in the production of important chemicals in the brain. In the treatment of ASD, P5P is given together with magnesium, an essential mineral necessary for the health of every cell in the body, including the proper functioning of brain and muscle cells. P5P is also important in methylation. (footnote 5)

Studies have shown that P5P and magnesium have significant positive effects on behavior in some autistic children.

Magnesium. Levels of this mineral are often low in children with behavioral, cognitive, and mood disorders. Magnesium deficiency symptoms include: anxiety or depression; constipation; muscle jerks, spasms, and tics; and poor appetite.

Magnesium is important in methylation and sulfation. (footnote 6)

Digestive enzymes. A lack of digestive enzymes may make it difficult to break down gluten and dairy products, or to metabolize proteins and fatty acids, leading to a condition known as “leaky gut.†Digestive enzymes, especially DPP-4, do not occur naturally in autistic children. Using them can increase tolerance to foods that might otherwise trigger symptoms of autism, such as aggressive or harmful behavior.

DPP-IV. A protein/enzyme, dipeptidyl peptidase IV, called DPP IV, helps digest casein and gluten. However, DPP IV has many different functions in the body besides digesting gluten and casein. This protein is known to influence T cells of the immune system. It is also a binding protein for purine, and adenosyl deaminase. Because of this, a problem with DPP IV can throw off the immune system, the amino acid profile, and methylation. In autistic patients allergic to casein and gluten, DPP-IV helps relieve stomach indigestion, gas, bloating, constipation, and diarrhea.

Vitamin E. A generic term for tocopherols and tocotrienols, vitamin E is a family of alpha, beta, gamma, and delta) tocopherols and corresponding four tocotrienols. Vitamin E is a fat-soluble antioxidant that stops the production of reactive oxygen species formed when fat undergoes oxidation. Of these, alpha tocopherol has been most studied as it has the highest bio-availability. But using alpha tocopherol alone leads to reduced serum gamma- and delta-tocopherol concentrations, so I give vitamin E in mixed tocopherols to obtain the greatest therapeutic benefit.

In autism, verbal apraxia is a common speech disorder. An estimated 50 per cent of children with autism have apraxia. According to new research published in the journal Alternative Therapies in Health and Medicine, daily supplements of vitamin E and Omega 3 fatty acids were associated with improvement in speech, imitation, eye contact, and behaviour.

Reportedly, 97 % of the participants with apraxia and/or on the autism spectrum reported dramatic improvements while taking this combination. The researchers discovered that they symptoms presented by children with apraxia mirror those of vitamin E deficiency. The study represents the largest summary of children with apraxia to date.

Omega 3 fatty acids. Considered essential fatty acids, these substances are necessary for human health. But the body cannot make them; they must be obtained through food. Omega-3 fatty acids can be found in fish, such as salmon, tuna, and halibut, other seafood including algae and krill, some plants, and nut oils. Also known as polyunsaturated fatty acids (PUFAs), omega-3 fatty acids play a crucial role in brain function as well as normal growth and development. I use krill oil because it contains anti-oxidants.

Omega-3 fatty acids are highly concentrated in the brain and appear to be important for cognitive (brain memory and performance) and behavioral function. In fact, infants who do not get enough omega-3 fatty acids from their mothers during pregnancy are at risk for developing vision and nerve problems. Symptoms of omega-3 fatty acid deficiency include fatigue, poor memory, dry skin, heart problems, mood swings or depression, and poor circulation. Together with Vitamin E, Omega -3 fatty acids improve speech.

Zinc. This element is typically deficient among autistic children. (One study of children with autism showed that 85% had low zinc levels.) Zinc deficiency impairs digestion, immune response, and methylation; it can also contribute to excessive levels of copper, which can be neurotoxic. Zinc deficiency often occurs because of gastrointestinal tract dysfunction. A major advantage of zinc supplementation is that it tends to increase the desire of autistic children to eat a wider range of food, in contrast to their usual limited preferences.

Calcium. Often deficient in ASD patients because of poor absorption or low dietary intake, this mineral may play a significant role in autism. Recent studies have suggested that a common variant of a gene called CACNA1G — which makes a channel that helps regulate calcium flow between cells — may increase the risk of developing autism. Because boys are more likely to carry the variant than girls, the finding could partially explain the disorder’s strong male bias.

Calcium channels are the cellular gatekeepers of calcium ions, which are required for muscle cells to contract and brain cells to fire. The new findings bolster emerging evidence that these channels play a critical role in autism and other neurological disorders.

Melatonin. Studies have shown that as many as 70% of children with autism suffer from sleep problems. Research points to a deficiency of melatonin — the body’s natural sleep hormone — as a likely cause. Secreted at night by the pineal gland in the brain, melatonin is thought to control sleep cycles, which are frequently disturbed in autistic children.

Vitamin C. A double blind 10-week trial reported excellent results in reduction of symptom severity with the use of 1 gram of vitamin C for every 20 lbs. of body weight. It may be that this positive benefit was a result of the well understood affects vitamin C has on a hormonal pathway typically damaged in autistic children.

Liposomal Vitamin C. Regular vitamin C is absorbed at approximately 19%, the balance remains in the gastrointestinal tract to attract water and loosen the bowels. Liposomalized vitamin C is absorbed at 93%, measurable in the blood stream, enhancing the anti-oxidant activity of vitamin C.

Oxytocin. A hormone that has effects on brain function, Oxytocin is best known for its role in facilitating labor, delivery, and breast-feeding. It is also important in promoting trust, love, and social recognition. Autistic children tend to have low levels of oxytocin. Studies have shown that oxytocin, used as a nasal spray, can significantly improve many symptoms associated with autism. I frequently use oxytocin and obtain impressive results.

Folinic Acid. Folate, folic acid and folinic acid are all forms of a water-soluble B vitamin. Folinic acid is used to promote higher levels of glutathione in individuals with autism. It plays a vital role in methylation.

Third Tier (and sometimes Fourth Tier)

DMG. A metabolic enhancer, N-Dimethylglycine (DMG) makes the process of metabolism (breaking down or building up of compounds in the body) quicker and more efficient. DMG also improves oxygen utilization, detoxification, cell protection, immune system modulation, and enhances healing. In autism, DMG acts as a methyl donor, adaptogen, as well as impacting the immune response, and enhancing neurotransmitter production. Its most important role is in the methylation pathway. It is a completely safe hypoallergenic nutrient.

TMG. An extract from sugar beets Trimethylglycine (TMG) is a natural polysaccharide and a good source of methyl groups that promotes healthier levels of the powerful pro-oxidant and free radical generator homocysteine. (Homocysteine is a toxic end product of the methylation of methionine, an essential amino acid.) TMG is also known as “Betaine.â€In Autism, TMG improves verbal communication, social interaction, lethargy, and may reduce seizures.

Creatine. A nitrogenous organic acid that occurs naturally in vertebrates, Creatine especially helps supply energy to muscle cells. It is essential for energy storage and transfer. Creatine can be very useful for children who suffer from low energy, low muscle tone, lethargy and expressive language delays.

Carnosine. A naturally occurring amino acid found in high concentrations in muscle, heart and brain tissues, L-Carnosine possesses powerful antioxidant, free radical scavenging and neurotransmitter properties. In a recent investigation, researchers treated 31 autistic children, ranging from 3 to 12 years in age, with either 400 mg of L-Carnosine, twice a day, or a placebo, for 8 weeks. At the end of the study the children treated with L-Carnosine showed significant improvements in behavior, socialization, and communication, as well as increases in language comprehension and expressive language. L-Carnosine is considered an extremely non-toxic and safe substance. As with other antioxidants, it acts synergistically when taken with other antioxidants.

CoQ10. Coenzyme Q10 (CoQ10) is an oil-soluble vitamin-like substance that can act as an antioxidant in the body. The Mayo Clinic says that the Coenzyme Q10 is recommended for a number of conditions. For instance, it is an acknowledged medication for mitochondrial disorders and for its benefits for people with congestive heart failure.

Most recently, CoQ10 has been used to treat brain disorders and neuro-degenerative diseases. It has been observed that autistic children have low levels of CoQ10. Since it works as an antioxidant, CoQ10 protects the brain by scavenging free radicals. It is known is that these free radicals can harm children with autism; they need CoQ10 supplements since, as mentioned earlier, they have very low levels of this enzyme.

Inositol. A naturally occurring nutrient found in various forms, the most common being myo-inositol. Inositol is found in phospholipids which function as cellular mediators of signal transduction, in metabolic regulation, and growth. Humans can make inositol in the body, which they do from glucose. Even though inositol is sometimes referred to as a vitamin, it is not a vitamin for humans.

A considerable body of research is accumulating that Inositol plays an important role in treating mental illnesses. Inositol is likely involved in signal transduction pathways involving serotonin, a neurotransmitter that becomes out of balance in several of these illnesses. Inositol’s efficacy in the absence of side effects makes it an attractive addition to treatment plans for specific mood disorders.

Studies have indicated that inositol helps with depression, anxiety, and OCD ( ). I’ve seen excellent results with inositol in children with autism or ASD in anxiety, hyper-activity, OCD symptoms and ADD ( ) symptoms.

Chelation. Where tests indicate the presence of toxic heavy metals in autistic children, I use chelation (with EDTA, DMSA, or both chelating agents) to remove traces of these metals. Chelation can be done orally, through a cream, or by suppository.

Pro-immune. This compound increases glutathione production. In autism, glutathione reserves are commonly low. This leads to an inability in many autistic-children to detoxify toxins - such as mercury and lead. These toxins adversely affect chemicals in the brain that support attention, focusing, and general awareness.

HERBAL TREATMENTS

Curcumin. Children on the Autism spectrum have shown improvements with the use of substances that have curcumin as their active ingredients. One reason for this improvement could be because curcumin has been shown to have both anti-bacterial as well as anti-fungal effects in the body. Curcumin also has been shown to be an effective anti-inflammatory, which can be very helpful for many children with Autism. In addition, based on mounting evidence, curcumin may also raise glutathione levels. These are among a number of reasons that curcumin-containing supplements could be helpful for children on the Autism spectrum.

Luteolin. A plant flavonoid, luteolin is known to impede the inflammatory response in several types of cells, including certain brain cells. Researchers first studied the effect of luteolin on microglia. These brain cells are a key component of the immune defense. When infection occurs anywhere in the body, microglia respond by producing inflammatory cytokines, chemical messengers that act in the brain to orchestrate a whole-body response that helps fight the invading microorganism.

This response is associated with many of the most obvious symptoms of illness: sleepiness, loss of appetite, fever and lethargy, and sometimes a temporary diminution of learning and memory. Neuroinflammation can also lead some neurons to self-destruct, with potentially disastrous consequences if it goes too far.

MEDICATIONS

Nootropic Piracitam. Scientists in Belgium first synthesized Piracetam in 1964. They were struck by its apparent ability to boost mental functioning in even healthy individuals and by its safety. Today, it is used as a treatment for childhood autism, a practice supported by clinical research. (Akhondzadeh, S et al, A double-blind placebo controlled trial of piracetam added to risperidone in patients with autistic disorder. Child Psychiatry and Human Development, Vol 39(3), Sep, 2008. pp. 237-245.)

Broadly speaking, nootropics (also referred to as smart drugs, memory enhancers, and cognitive enhancers), are drugs, supplements, nutraceuticals, and functional foods that appear to improve memory, intelligence, motivation, attention, and concentration. The word nootropic was coined in 1972 by the Romanian Dr. Corneliu E. Giurgea from Greek words mean “mind†and “to bend/turn.†Nootropics are thought to work by altering the availability of the brain’s supply of neurochemicals (neurotransmitters, enzymes, and hormones), by improving the brain’s oxygen supply, or by stimulating nerve growth.

Hydergine. As with most other cognitive enhancing drugs, hydergine was originally intended as a treatment for people with various neurological or mental deficiencies or diseases. Hydergine works by dilating the blood vessels of the brain, allowing more oxygen to be delivered to neurons and other brain cells.

Valtrex. An anti-viral drug, Valaciclovir is used in the management of certain forms of herpes virus. It is marketed under the trade name Valtrex.

Actos. (Reduces brain inflammation, especially glial cells).

Exelon. (I use it because I’ve found that it improves neuronal function.)

Minocycline. (Weak antibiotic shown to reduce inflammation in astrocyte cells in brain.)

Aldactone. (Also reduces brain inflammation.)

Naltrexone. Research has shown that many autistic individuals have high levels of beta-endorphins in their central nervous system. Low dose naltrexone blocks the action of opiate receptors, thus reducing their level of endorphins. Improvements noted in autistic individuals who have taken low dose naltrexone include: increased socialization, eye contact, and general happiness; normalized pain sensitivity; and a reduction in self-injury and stereotypic (self-stimulatory) behaviors.

There are no known side-effects of low dose naltrexone.

Diflucan. Autistic symptoms are made worse by the overgrowth of Candida albicans, a yeast-like fungus. Overgrowth is made possible by a dysfunctional immune system. Many children afflicted with autism have had frequent ear infections as young children and have taken large amounts of antibiotics. These are thought to exaggerate the yeast problem. Other possible contributors to Candida overgrowth are hormonal treatments; immuno-suppresant drug therapy; exposure to herpes, chicken pox, or other “chronic†viruses; or exposure to chemicals that might upset the immune system. There is an increased probability, that a “general†environmental factor affecting our immune systems (i.e. ozone layer depletion, “toxic†chemicals, etc.) may be operative, affecting many children and adults.

Treatment with Diflucan, a potent anti-fungal, will cause most of the yeast to die off within two months (sometimes within a month). If the treatment is successful for autistic children, usually eye-contact improves and the child seems more aware and less “foggy.†Anecdotal reports claim that the frequency of inappropriate noises, teeth grinding, biting, hitting, hyperactivity, and aggressive behavior decreases. The child acts less silly and shows less inappropriate laughter.

Ritalin and Abilify. (Infrequently and in low doses.)

Anti-seizure Medication. A small but significant number of my autistic patients have seizures. But in some of these patients, the seizures (not noticeable). But these silent seizures can be causing delayed speech and other symptoms of autisms.

OTHER IMPORTANT TREATMENTS

Hyperbaric oxygen therapy. A randomized, double-blind controlled study of 62 children found that those who received 40 hours of hyperbaric oxygen therapy over a month were less irritable, more responsive when people spoke to them, made more eye contact and were more sociable than kids who didn’t receive it. They were also less sensitive to noise (some autistic children experience a kind of sensory overload from loud sounds and background noise). The greatest improvement was observed in kids older than five (the study included children ages two to seven) who had milder autism.

Note: I have a hyperbaric chamber in my office.

Note. Some substances chiefly appropriate for tiers two or three can be used in both tiers.

As I stated at the beginning of this article, my treatment program has helped hundreds of autistic children. It can also help your child. To make an appointment, phone .

FOOTNOTES

1. Liver function test. Most people with ASD’s have compromised liver function. When something is going awry in the liver, other systems are affected and the liver is left far more vulnerable to toxicity by many substances; including prescription and over-the-counter medications.

2. Vitamin and essential nutrient blood test. Studies suggest that intestinal disorders and chronic gastrointestinal inflammation may reduce the absorption of essential nutrients and cause disruptions in immune and general metabolic functions that are dependent upon these essential vitamins. Other studies have shown that some children on the autism spectrum may have low levels of vitamins A, B1, B3, and B5, as well as biotin, selenium, zinc, and magnesium; while others may have an elevated serum copper to plasma zinc ratio, suggesting that they may benefit by avoiding copper and taking extra zinc to boost their immune system. Other studies have indicated a need for more calcium. Perhaps the most common vitamin supplement used for individuals with ASD is vitamin B, which plays an important role in creating enzymes needed by the brain. In several studies on the use of vitamin B and magnesium (which is needed to make vitamin B effective),

almost half of the individuals with autism showed improvement. The benefits include decreased behavioral problems, improved eye contact, better attention span, and improvements in learning. Other research studies have shown that other supplements may help symptoms as well. Cod liver oil supplements (rich in vitamins A and D) have resulted in improved eye contact and behavior of children with autism. Vitamin C helps in brain function and deficiency symptoms like depression and confusion. Increasing vitamin C has been shown in a clinical trial to improve symptom severity in children with ASD.

3. IgG food allergy test. Immunoglobulin G (IgG) are antibodies that provide long term resistance to infections. The complete elimination of IgG positive foods may bring about important improvements in symptoms of autism and AD(H)D, as demonstrated in numerous clinical studies. The 93 foods tested in the IgG Food Allergy Test increase the identification of numerous offending foods. This test can be performed using either serum from a blood draw or dried blood from a finger prick.

4. Porphyrins. Pigments found in both animal and plant life, porphyrins are all chelates with metal. These chemicals are important in making red blood cells and carrying oxygen throughout the body. The body uses enzymes to convert porphyrins into heme. (Heme is found in all body tissues, with the largest amounts in red blood cells, bone marrow, and the liver.)

Recent studies, conducted in three separate continents, have examined urinary porphyrin profiles in ASDs. In each of the studies, mercury-associated urinary porphyrin profiles were found to be significantly increased across the autism spectrum, from mild to severe ASD diagnoses. Previous studies also demonstrated that chelation therapy in ASDs resulted in significant reductions in mercury-associated urinary porphyrin profiles. Furthermore, using the Childhood Autism Rating Scale, a recognized test of ASD severity, researchers found a significant increasing correlation between mercury-associated urinary porphyrin profiles and Childhood Autism Rating Scale scores prior to blinded laboratory testing. Providing further support for these correlations, other studies have shown that ASDs, relative to controls, had increased: brain mercury levels; blood mercury levels; mercury levels in baby teeth; and mercury in the urine/fecal samples

following chelation therapy; as well as decreased excretion of mercury through first baby haircuts.

5. Methylation. An important metabolic process, defective in autism, Methylation pertains to the control of histamine excess, protection of DNA, promotion of serotonin production, and other brain functions. A number of experiments have suggested a relationship between methyl group metabolism and the exocrine secretion of the pancreas. These included nutritional studies which showed that ethionine, the ethyl analog of methionine which inhibits cellular methylation reactions, is a specific pancreatic toxin.

6. Sulfation. People with autism were found to excrete roughly twice as much sulfate in their urine, so that they had only 1/5 the normal level of sulfate in their bodies. Sulfur is an essential mineral, and is needed for many functions in the body. AIDS patients have also been found to exhibit a loss of sulfur in their urine, leading to a loss of extracellular sulfated structures in the brain. This has not yet been investigated in autism, but may be the same.

Love, Gabby. :0)

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"I know of nobody who is purely Autistic or purely neurotypical. Even God had some Autistic moments, which is why the planets all spin." ~ Jerry Newport