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 Comprehensive Guide to Managing Autism 

Willis S. Langford 

Slightly changed by Kees de Vries, Drunen, Holland (june 2003) 
 
Warning: Do not scan and read this paper piecemeal. It must be studied to avoid mis-steps.

Introduction

There are several very basic things discussed in this paper that can be done at home with little or no expensive testing. Foremost is the home testing for thyroid function discussed toward the end of this paper, and support of thyroid function. The “unloading of the donkey” is vital to possibly 80% of these troubled children for they are poisoned, drowning in their own toxic wastes. Elimination of bowel disorders is very first on the list of vital action. It is often as simple as supplying a digestive enzyme supplement, or removing milk. Some autistic children can be helped dramatically by medical procedures such as an infusion of the intestinal hormone secretin. The need and the beneficial response to secretin, I think, are dependent upon the amount of damage to the duodenum and small intestine from whatever cause, and on the stomach’s ability to produce adequate hydrochloric acid (HCl) for proper digestion. Since proper functionality of these two things largely determine proper digestion, it is vital that both be operative. Without adequate HCl, secretin infusion can, at best, be only partially effective in restoring digestion and proper physical and mental function. Secretin is reduced in hypothyroid rats (Robberecht et al, 1981), so first support the thyroid. HCl production is very dependent on adequate zinc levels, usually lacking in these children. With support for the thyroid, adequate zinc, and possibly supplemental betaine hydrochloride, secretin infusion may be totally unnecessary. 

The path of autism is different for each child. Some are prone to seizures, some are not; some behave aggressively while others are overly passive. However, children with autism and with ADHD share several factors. There is a deep disturbance in their fatty acid metabolism that impairs their utilization of amino acids, and often there is an imbalance in their electrolytes. Electrolytes control what’s called membrane traffic—what goes in and out of cells. This means that providing other nutritional supplements is relatively ineffective until the electrolyte (sodium-potassium-magnesium-calcium) imbalance is corrected. The delicate balance of electrolytes also controls the electrical activity within the brain. Practitioners suggest the extent of the nutritional problem in these observations:  

Nutritional abnormalities: 

a. Zinc deficiency exists in 90% of autistic children

b. Copper excess exists in 85%

c. Calcium and magnesium deficiencies are common

d. Omega 3 fatty acid deficiency exists in nearly 100%

e. Fiber deficiency exists in nearly 100%

f. Antioxidant deficiency exists in nearly 100% 

Additionally, there is heavy metals poisoning: A recent study found 85 percent exhibited severely elevated Copper/Zinc (Cu/Zn) ratios in blood, suggesting a disorder of metallothionein (MT), a short, linear protein responsible for homeostasis of copper and zinc and many other metals. “The severity of the Cu/Zn imbalance was far greater than that of any other population we have studied over the past 25 years,” said William J. Walsh, Ph.D., Physician, biochemist and chief scientist of the Pfeiffer Treatment Center, Naperville, Illinois. His database suggests that copper overload and zinc depletion are the most common metal-metabolism abnormalities in behavioral conditions such as, ADHD, autism, depression, bipolar disorders, and schizophrenia. In addition, these sufferers are unusually sensitive to lead, cadmium, mercury, and other toxic metals that they tend to accumulate rather than eliminate. Nevertheless, if a mouse cannot make MT, then it should not get copper deficient when fed a high-zinc diet. We fed some of these mice and some control mice (ones that can make MT) diets that contained normal amounts of zinc and some that contained much more zinc. The results showed that the mouse without MT got copper deficient when fed the same high-zinc diet as the mouse that had MT. This study strongly suggests that the old theory is not true and that stimulation of MT is not necessary for high-zinc to bring about a copper deficiency. We suggest instead that the high zinc is inhibiting a copper transport protein in the intestinal membrane, and copper cannot be absorbed—Reeves PG, Copper Metabolism in Metallothionein-null Mice Fed a High-zinc Diet. J Nutr Biochem 9:598-601, 1998.  

Blood and urine analyses yielded evidence of a metallothionein dysfunction in 499 of 503 patients (99%) diagnosed with autism spectrum disorders, according to Walsh, suggesting that autism may be caused by either a genetic MT defect or a biochemical abnormality, which disables MT protein. “An MT disorder may affect the development of brain neurons and may cause impairments in the immune system and gastrointestinal tract, along with hypersensitivity to toxic metals,” he said. The excess copper in these kids is probably from two causes. Mercury depresses zinc, and there is a high incidence of zinc malabsorption. To reduce copper, you must use significant amounts of vitamin C and zinc.  

Treatment for this imbalance centers on stimulation of MT protein with divalent metals (such as zinc and manganese) that are in depletion, and by providing N-acetylcysteine, serine, selenium, and other constitituents of MT. Of secondary benefit are vitamins B6, A, C, D, E, glutathione, genistein and biochanin A (both from soy), and glucocorticoids (anti-inflammatory drugs). This treatment should be gradual during the first 4 weeks of treatment to avoid rapid release of copper from tissues, which could cause a sudden worsening of symptoms. 

Mercury adversely affects detoxification systems such as metallothionein, cytochrome P-450 (Phase I), and bile. Mercury ties up this material so it cannot bind and clear other metals such as lead, cadmium, and aluminum. Mercury inhibits sulfur ligands in MT and, in the case of intestinal cell membranes, inactivates MT that normally binds cuprous ions, thus allowing buildup of copper to toxic levels and malfunction of the zinc and copper containing Super Oxide Dismutase (SOD). Mercury induced reactive oxygen species and lipid peroxidation (forming free radicals) has been found to be a major factor in mercury’s neurotoxicity, along with its leading to decreased levels of the vital enzymes glutathione peroxidase and superoxide dismustase (SOD).  

Metallothioneins across species are rich in cysteine (~30%) and have higher affinities for mercury (Hg) and cadmium (Cd) than for zinc. Therefore, as Hg and Cd bind to metallothionein, and are restricted from entering the mitochondria, zinc is released. The free, ionized zinc, which would be toxic if permitted to accumulate, binds to a metal regulatory element on the promoter region of the metallothionein gene and “turns on” the synthesis of metallothionein. Increases of as much as 3-times are reported. Such induction of metallothionein provides increased binding capacity for both toxic metals (protective) and zinc (functional). The displacement of zinc in the presence of toxic metal burden may explain in part why increased levels of zinc are so commonly seen in the scalp hair of patients exhibiting significant levels of toxic metals Hg, Cd, Pb (Quig, unpublished observations). 

Furthermore, their minerals and amino acids are deficient and/or imbalanced. Their production of red and white blood cells is irregular. They have a dysfunctional immune system (often attacking “self”). Eighty percent suffer mitochondrial disorders (lack of energy production) according to Dr. Colemen, George Washington University Hospital. Ninety percent suffer some degree of hypothyroidism despite “normal” TSH readings (Raphael Kellman, MD). Eighty-three percent suffer dysfunctional Phase I and II, liver-enzyme activity (causing a build up of toxins and heavy metals), and 85% of autistic meet criteria for malabsorption leading to a multitude of nutrient deficiencies (Wm. Walsh). Both the autistic and the ADHD children often suffer lymphoid modular hyperplasia (measles infection in the gut—Wakefield). Thus, children with autism do not absorb food properly, leading to nutrient deficiencies. The most common deficiencies of poor diet and malabsorption are fatty acids, the minerals zinc, selenium, magnesium, and calcium, and the vitamins A, B6, C, and D, and E. This compromises immune function, and provides inadequate antioxidant protection to offset the high oxidative stress these children suffer, thus causing significant damage to cells throughout the body and brain. It is interesting to note that uric acid plays a key antioxidant role in the plasma, and many of these children have low urea/uric acid, possibly reflecting high oxidative stress. The nutrient deficiencies can occasionally cause extreme behaviors; some children with autism have been reported to have actually gouged out their eyes due to a calcium deficit. If your child is pushing at his eyes, supplement calcium and vitamin D, and get him in the sun.  

Children with autism have a lot of metabolic abnormalities as indicated, but that is a result of the problems with their immune system. Heavy metals such as mercury induce a dramatic activation of the immune system and autoantibody production in the genetically susceptible. This autoimmune syndrome is dependent on T-Cells, which are important for B-Cell activation and cytokine secretion. Studies have found mercury impairs the body’s ability to kill Candida albicans by impairment of the lytic activity of neutrophils. A population of plant workers with average mercury excretion of 20 ug/g creatinine was found to have long-lasting impairment of neutrophil function. 

Another study found such impairment of neutrophils decreases the body’s ability to combat viruses such as those that cause heart damage, resulting in more inflammatory damage. Samplings of immune data reveal that most of these autism-spectrum disorder (ASD) children have atypical elevations of antibodies against otherwise common pathogens such as Epstein-Barr virus, Cytomegalovirus, and/or Human Herpes Virus 6 (EBV, CMV, HHV-6), and in some 30%, elevated anti-measles antibodies indicative of chronic infection from measles vaccine—Kawashima H, Mori T, Kashiwagi Y, Takekuma K, Hoshika A, Wakefield A; Department of Paediatrics, Tokyo Medical University, Japan. “Of the 160 autistic children we looked at, only five did not have bowel disease”—Wakefield. (Attenuated vaccines contain live viruses that don’t usually cause overt disease.) HHV-6 induces synthesis of a broad range of host cell proteins, including interferon alpha, CD4, interleukin-1 beta, and tumor necrosis factor alpha.  Additionally, HHV-6 kills Natural Killer Cells. 

Human herpesvirus-6, the etiologic (causative) agent of roseola, is ubiquitous, establishes latency in the host, and can infect a variety of immunocompetent cells, with CD4+ T lymphocytes being the targets in which it replicates most efficiently, and HHV-6 has an “Immunosuppressive effect... on T-cell functions” such as “suppression of interleukin-2 synthesis and cell proliferation.” 

HHV-6 is a commensal inhabitant of brains. Various neurologic manifestations, including convulsions and encephalitis, can occur during primary HHV-6 infection, or in immunocompromised patients. HHV6 has been reported within oligodendrocytes and microglia, and focal HHV6—encephalitis has been documented. It is considered causative in CFS. 

John O’Leary, Ph.D., a world-class researcher and molecular biologist from Ireland, using state of the art sequencing technology, showed how he had found measles virus in the gut of 96% of autistic children, compared to 6.6% of normal children. This virus did not come from the natural disease; it came from the measles vaccine. In addition, Dr. O’Leary found measles virus present in 75% of children with Crohn’s Disease. Crohn’s has traditionally been an intestinal disease of adults, following years of dietary abuse. Its appearance in children is a new event, and Dr. O’Leary’s work points to measles virus from vaccines as the likely cause. Additionally, Candida, according to antibody studies done at the Atkins Center, is involved in more than 80 percent of all cases of Crohn's and Colitis. 

Their pathogenic (disease producing) power is derived from the fact that they can set up persistent infections within various lymph tissues (that of the gut, for example, as shown by Wakefield) as well as within circulating cells of the immune system. Wakefield found that controls had prevalence in the gut of HHV-6 DNA similar to that of those with ulcerative colitis—86%! Virus infected monocytes (White Cells) travel freely throughout the body, and have been shown to enter the brain, take up residence there, and secrete cytokines (chemical messengers) toxic to brain tissue. They also serve as foci of infection. It is not uncommon for infants to run fevers and show other signs of acute inflammation after receiving multiple vaccinations. Interferon production is stimulated by infection with a virus to protect the body from super infection by some other microorganism. In this study, vaccination of one-year-old infants with measles vaccine caused a precipitous drop in the level of alpha-interferon produced by lymphocytes. This decline persisted for one year following vaccination, at which time the experiment was terminated—Journal of Infectious Diseases. Thus, this study showed that measles vaccine produced a significant long-term immune suppression. Similarly, the report in the British medical journal Lancet confirmed that a significantly higher percentage of these children had received a DTP shot within 30 days of the onset of polio compared to a control group of children without polio, 43 percent of polio victims compared to 28 percent of controls. The DTP vaccine suppresses the body’s ability to fight off the polio virus. Thus, we have evidence of long-term damage to the immune system from vaccines. Starting at about 4 months, this leads to the infections, antibiotics, more infections, and more vaccines that often precede autism. 

“Complete Immunoglobulin E (IgE) deficiency was seen in 10% of the patients. Almost 20% of the patients had low IgA, and 8% of them had a complete lack of it, which is quite high compared to the general population (1 in 700-1,000). About 25% of the subjects had IgG subclass deficiency. About 25% of the patients had a deficiency of various subsets of lymphocytes (e.g., CD3, CD4, and CD8 Killer T-Cells). In fact, almost 35% of these autistic children had a deficiency in Natural Killer Cells. In general, the cytokines IL-2 and alpha-interferon are increased, while IL-1 is normal”—Dr. Sudhir Gupta. IgG anti-brain autoantibodies were present in 27% with ASD, and with 2% from healthy children. IgM autoantibodies were present in 36% with ASD compared with 0% of controls. The presence of these antibodies raises the possibility that autoimmunity plays a role in the pathogenesis of language and social developmental abnormalities in a subset of children with these disorders—Serum autoantibodies to brain in Landau-Kleffner variant, autism, and other neurologic disorders. J Pediatr 1999 May;134(5):607-13.  

“I firmly believe that up to eighty percent (and possibly all) cases of autism are caused by an abnormal immune reaction, commonly known as autoimmunity. The autoimmune process in autism results from a complex interaction between the immune system and the nervous system.  

“Antibodies to measles (rubeola) virus (MV) and human herpes virus-6 (HHV-6) are elevated, which is a sign of a present infection, past infection, or a reaction to the measles-mumps-rubella (MMR) vaccine. The HHV-6 and measles viruses are etiologically linked to autism because they are related to brain autoantibodies and demyelinating diseases.  

“Recently, I conducted a study of measles virus (MV) and HHV-6 in autism....This study showed two things in particular: first, that the virus antibody levels in the blood of autistic children were much higher when compared to normal children; and secondly, the elevated virus antibody levels were associated with the brain autoantibody titer. Interestingly, the viral antibody and brain autoantibody association was particularly true of MV antibody and Myelin-Basic Protein (MBP) autoantibody (i.e., 90 percent of autistic children showed this association). This observation led me to hypothesize that a measles virus-induced autoimmune response is a causal factor in autism, whereas HHV-6, via co-infection, may contribute to the pathophysiology of the disorder. Although as yet unproven, I think it is an excellent working hypothesis to explain autism, and it may also help us understand why some children show autistic regression after the measles-mumps-rubella (MMR) immunization. 

“There is enormous potential for restoring brain function in autistic children and adults through immunology....The goal of therapy should be to normalize or reconstitute the immune response instead of inducing immune suppression or stimulation. This will maintain a balance within the normal immune response, avoiding major fluctuations of overt immune activity which could be detrimental to the patient”—Excerpts from Autism, Autoimmunity, and Immunotherapy: a Commentary by Vijendra K. Singh, Ph.D. Department of Biology & Biotechnology Center, Utah State University, Logan Scientific Board Member, Autism Autoimmunity Project. 

Reed Warren, et al, mention how the IgA findings relate to infections and report a fascinating double susceptibility in that 6 of 8 autistic kids with low IgA levels also had null alleles of the complement C4b: “...IgA is also important in protection against pathogenic infections and participates in the clearance of pathogens via the alternative complement pathway. C4 proteins [e.g., from the C4a and C4b genes] are involved in the other complement pathway, the classical complement pathway. Therefore, it is interesting that of the eight autistic subjects with decreased IgA levels, all but two also had a C4b null allele suggesting that, in these patients, both pathways of complement activation [and response to infections] are probably operating at less than optimal level.”   

A test of thirty-six children revealed grade I or II reflux esophagitis in 25 (69.4%), chronic gastritis in 15 (42%), and chronic duodenitis in 24 (67%). Low intestinal carbohydrate digestive enzyme activity was reported in 21 children (58.3%), although there was no abnormality found in pancreatic function. Seventy-five percent of the autistic children had an increased pancreatico-biliary fluid output after intravenous secretin administration (indicating hypersensitivity of the pancreas) —Gastrointestinal abnormalities in children with autistic disorder. J Pediatr 1999 Nov;135(5):559-63. 

Children with autism produce higher levels of pro-inflammatory cytokines than children without autism. Autistic children have been shown to exhibit many anomalies in cell-mediated immunity, including abnormal T-cell activation (Warren et al, 1995), decreased relative numbers of helper-inducer lymphocytes, and a lower helper-suppressor ratio. (Denney et al, 1996) These last 2 measures were inversely correlated with severity of autistic symptoms. In children with these abnormal antibody patterns, selenium supplementation at a dose of 10 mcg/kg body weight for six months significantly increased IgG-2 and IgG-4 levels and reduced the number of infections. Low blood values of these two antibodies are associated with intractable seizures. Selenium and vitamin E supplementation has overcome intractable seizures that were resistant to drugs.  

In workers exposed to fluorine, those with subclinical hypothyrosis [reduced tri-iodothyronine (T3) in 51%] had immune alterations that were more evident. T-lymphocytes count rose, but their functional activity declined, indicating impaired cooperation of immunocytes as a result of imperfect control under low concentrations of T3 (Balabolkin, 1995). Their immune system is driving with no brakes!  

Elevated serotonin levels have been consistently found in 30% -50% of autistic patients, and may represent a marker for familial autism. Hyperserotonemia in autism appears to be due to enhanced 5-HT uptake, as free 5-HT levels are normal and the current report of an excess of the long/long 5-HTTLPR genotype in autism could provide a partial molecular explanation for high platelet serotonin content in autism—PMID: 11378854. Serotonin synthesis is decreased in the brains of autistic children and increased in autistic adults, relative to age-matched controls (Chugani et al, 1999), while whole blood serotonin in platelets is elevated regardless of age (Leboyer; Cook, 1990).  

Finally, these kids are hypersensitive to everything: sound, light, touch, and colors. Typically, bright yellow will drive them up the wall leading to all sorts of aberrant behavior. This sensitivity is usually related to a deficiency of vitamin B6, zinc, and magnesium.  

These medical facts show that every symptom of these dear children is treatable! These kids are sick. They are not usually brain damaged. What seems to be occurring is an immune mediated, abnormal “shut down” of blood flow in the temporal lobe area of the brain, and therefore an interference with central nervous system function. 

This paper is not meant as a medical prescription, nor do all the conditions and suggested interventions apply to every child. You must study this paper until you see your child’s face in it, and then use the parts that are applicable to him. In all instances, it is good to consult with your medical professional when making any major nutritional changes. 

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