Lower Autism Treatment Evaluation Scores (ATEC) correlate with dietary transfer factor use in autism spectrum disorders (ASDs), pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS), and primary immunodeficiency (PI) disease/CD19 defect: Two case studies. By Suzette Lawrence, MSN, CNM

n 1949, Dr. Sherwood Lawrence conducted a landmark study that demonstrated that immunity is transferable in a small compound found in white blood cells. Dr. Lawrence was able to transfer the immune memory (not the disease but protection

from it) of tuberculosis (TB) in a substance in lymphocytes (white blood cells) to a person who had no such immune recognition abilities. The recipients became skin test positive for TB in a matter of days indicating that the recipients had adopted the immune recognition capabilities for TB from the donors. This was achieved without suffering the illness or the primary immune response. Lawrence was able to transfer immune memory, hence the name “transfer factor.”

What are transfer factors (TFs) and how do they influence immune system function?Structurally TFs are polypeptides or chains of specific amino acids that encode the identity of specific microbes and, therefore, educate the immune system to recognize the correlating disease causing organism (Kirkpatrick, 2000). TFs are the reason that most infections confer some measure of future immunity. The influence of transfer factors on immune system function extends to a general ability to improve immune system readiness by improving the activity and proliferation of natural killer (NK) cells (Lang, 1982) (Kisielevsky, Khalturina, 2005). NK cells are a subset of immune cells that differentiate self from non-self. NK cells identify and destroy cells that are infected with viruses and bacteria as well as cancer cells (see Khemka, Sahl, Bui, Tilles, 1997; Imai, Matsuyama, Miyake, Suga, Nakachi, 2000). When NK cell function is strong, we expect less illness, and when we do get sick, we expect to

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be able to recover naturally. Dr. David Markowitz’s clinical experience supports this expectation. He reported an 82-85% reduction in antibiotic use and a 75% reduction in illness in his pediatric patients who used TF over a 6-month period. He collected data during a 7-year period, from 1999 to 2006, in over 680 patients in an age matched retrospective clinical observation. (David Markowitz, MD, personal communication, April, 28, 2010).

Dietary TF has also been shown to improve salivary immune globulin A (sIgA) in healthy adults (Bennett, Vaughn, Lefler, McCausland, Lisonbee, 2009). This research supports anecdotal reports of improvement in sIgA in children with ASD and supports the wider influence of TF in immune system function. SIgA is the first line antibody defense of the upper respiratory system, the gastrointestinal tract, and all mucus membranes of the body (Corthesy, 2006).

Autism spectrum disorders, autoimmunity and dietary TFAutoimmunity is when the immune system loses its regulatory capacity. It begins to attack self instead of just non-self. ASD is described in the immunology literature as an autoimmune condition (Singh, 2009; Gupta, Aggarwal, Rashanavan, Lee, 2005). Autoimmunity in ASD may be expressed in high autoantibodies to the brain (Singh, Warren, Averett, Ghaziuddin, 1997; Singh, Jensen, 2003), and inflammation of the brain (Singh, 2005). Inflammation and immunopathology of the gastrointestinal tract have been established in children with ASD (Ashwood, Anthony, Pellicer, Torrrente, Walker-Smith, Wakefield, 2003; Ashwood, Anthony, Torrente, Wakefield , 2004). Autoimmunity has a chaotic effect on the immune response.

Suzette Lawrence, MSN, CNM, earned her bachelor’s degree in nursing from the University of Maryland at Baltimore and practiced high-risk labor and delivery there. She graduated Sigma Theta Tau from the University Of Texas School Of Nursing with a master’s degree (MSN). Concurrently, she earned the National Certification for Nurse Midwives (CNM) from Texas Tech University Health Sciences Center. Suzette went on to practice full-scope nurse midwifery in Denver, Colorado. In 1998, she joined 4Life Research (Sandy, Utah) as an independent representative for the transfer factor family of products. She is a founding member of the 4Life Research Health Sciences Advisory Board. She contributes to transfer factor research and product design. Suzette helps her clients to develop health, wellness and immune strengthening strategies. Her special area of interest is autism spectrum disorders (ASDs). www.suzettelawrence.com.

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Allergy, eczema, and asthma are all states of autoimmunity (Kidd, 2003). TF has a modulating effect on immune function (Dwyer, 1996; Vorobiev, 2004). The emerging science points to immune modulation, that is, the ability to upregulate or downregulate as a critical component to immune competence (R.H. Bennett, PhD personal communication, May, 20, 2004). For people contending with autoimmune conditions like ASD, PANDAS, or PI disease, this may be the most important contributing factor to success with this dietary supplement.

Where do TF molecules come from? TFs are naturally occurring molecules that are the same in all mammals. During pregnancy they are collected in the breast tissues of the parturient and secreted into colostrum at birth (Parley, Beer, 1976; France, Marmer, Steele, 1980). When the newborn nurses, his immature and naive immune system is educated by the maternal immune history via the TF molecule. This education trains the immune system to recognize, respond, remember, and regulate the newborn’s immune function. The immune-enhancing benefits of dietary TF are available to us at any age (Vorobiev).

Many children with ASD benefit from a gluten- and casein-free diet (GF/CF). TF is GF/CF. The large milk proteins naturally found in colostrum are removed through an ultra filtration process (Wilson and Paddock,1983). TF is typically suggested for people with ASD because it is a natural, gentle, effective, and well-tolerated immune modulator (Pizza, DiVinci, Fornarola, Parlareti, Baricirdi, Viza, 1996; Vorobiev; Bock, 2004). I suggest dose and product adjustments for the individual as parent interviews and reports indicate.

We use a series of ATEC reports to mark progress (www.autism.com/ind_atec_survey.asp). In these cases, the ATEC illustrates the range of influence that a functional immune system has on the central nervous system, far beyond resistance to colds and flu.

Dietary TF as a first biomedical intervention for a 46-month male with ASD/regression after vaccinationPA weighed 5 pounds 1 ounce and was

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Left: At the time of the ASD diagnosis Middle and right: PA Christmas 2004 at age 2 PA and his little brother Christmas 2009,

delivered at 37 weeks gestation via spontaneous vaginal birth. He was nursed for 5 months. PA’s paternal history is significant for allergy, rheumatoid arthritis, and lupus. Mom’s prenatal course was remarkable for extensive dental treatments for an abscessed tooth that included 30 days of antibiotic therapy. At 3 weeks of age, PA began suffering from colic and gastric cramping. PA was diagnosed and treated for croup at 10 months, double ear infection at 12 months requiring a 30-day course of antibiotics, upper respiratory infection at 14 months, herpangina at 16 months, constipation at 16 months and 1 week, streptococcus at 20 months, croup at 21 months and 1 week, and at 22 months asthma was ruled out.

Vaccination schedule stopped after 20 month shotsPA’s pediatrician was concerned about ASD by his 20-month well-baby visit on 8/11/04 and referred him to a Defeat Autism Now! (DAN!) doctor, where he received an autism diagnosis at 24 months of age. By 28 months he was receiving 20 hours a week of 1:1 applied behavioral analysis (ABA). PA was 46 months of age when immune modulation with dietary TF was instituted. At that time, PA’s ABA therapist completed a series of three autism Treatment Evaluation Checklists over a 20-week period to evaluate his progress. She was unfamiliar with TF and was uncertain of what to expect. PA was not on any medications and had not received any dietary supplements prior to supplementation with TF . He was on a regular diet. At the time PA began his 20-week trial with stress doses of the TF, these were his parents’ observations of greatest concern:

Birth 2 month 4 month 6 month 12 month 20 month 12/27/02 3/03/03 4/28/03 6/27/03 12/30/03 8/11/04 HepB HepB HepB Hib Hib Hib Hib DTaP DTaP DTaP DTaP IPV IPV IPV Varicella MMR Prevnar Prevnar Prevnar

Figure 1: Vaccine Chronology:

Delayed speech Constipation: 3-4 difficult

stools per week Eczema all over Unable to follow two-part

commands Didn’t jump with both feet Unable to have a

conversation Inconsistent eye contact Unable to potty train Covers ears with hands on

occasion Zones out and stares into

space Does not interact with

others often Sense of fear is absent

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PA’s ATEC scores dropped from a baseline of 35 to 4 during this first intervention with the TF product. His nearly neurotypical ATEC score was reflected in his daily life. He became a happier and healthier child. His eczema resolved and his recurring infectious illnesses abated. He potty trained during the second half of the trial. He was able to carry on a conversation and his sensitivities to noise resolved. He became more “connected” with our world and joined his neurotypical peers in 2008 in kindergarten. PA attends public school and is in the 90% percentile of his first grade class academically. In a follow-up interview for this publication, Mom reported PA is enjoying great health and a happy childhood with no special considerations regarding his former ASD status. PA’s maintenance regimen includes TF , probiotics, and digestive enzymes to support his excellent health. Antibiotics and antipyretics have not been prescribed since age 20 months.

NJ: A 16-year-old male with ASD, regression after vaccination, PANDAS, and PI disease/ CD19 defect.The pregnancy was significant for the treatment of two bladder infections. One in the first trimester was treated with Macrodantin, and one at 5 months was treated with amoxicillin. NJ was delivered spontaneously at 42 weeks gestation (2 weeks post due date). NJ weighted 9 lbs, his Apgar scores were 9/9. He was formula fed. NJ’s paternal history included anxiety, depression, ulcers, asthma, diabetes, and ulcerative colitis. NJ’s maternal history included ovarian cancer, recurrent sinusitis, arthritis, depression, ulcers, Crohn’s disease, ulcerative colitis and mood disorder.

Following delivery, NJ was a calm and beautiful baby who made eye contact with his mom. At 48 hours he received the hepatitis B vaccine and began crying. He cried for the next 3 weeks for about 18 hours a day. He was switched to a soy formula. He continued to cry. His demeanor improved by 8 weeks but eye contact was difficult to elicit. By 4 months his eye contact improved and Mother was less concerned until NJ suffered a pulmonary infection at 6 months of age. It was treated with erythromycin. At 9 months, he suffered the first of a series of nine ear infections. They occurred monthly and were treated with antibiotics. By the fall of 1995, he had his first set of ear tubes placed; these helped reduce ear infections to just three by the time they fell out for good at age 6. He suffered countless sinus infections during this time.

At 13 months he ran a fever after receiving the MMR. He looked dazed in his birthday pictures. At 15 months, NJ was diagnosed with rotavirus and was ill for 2 weeks; 1 month later the rotavirus was back. At 18 months, NJ received the chicken pox vaccine and developed a 105-106 degree fever within 4 hours. This continued for 48 hours despite alternating doses of ibuprofen and acetaminophen. His fever dropped to 103-104 degrees and his capillary refill time was

3-4 seconds. On day 3 he improved and broke out in a rash. Within 1 month, he was fully disengaged − no eye contact and no curiosity. Mom approached the pediatrician asking whether NJ was autistic. At 19 months NJ characterized autism. He received an ASD diagnosis at 30 months. At 30 months, Mom completed the Diagnostic Checklist for Behavior-Disturbed Children, Form E2 (1996), an early version of the ATEC currently in use at the Autism Research Institute, and he received a score of 8+ indicating that NJ was indeed autistic.

Mom hired a well-known and respected therapist, and

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*fever ** febrile seizure ***see text. 1m = 1 month

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a 30-hour per week in-home therapy plan was developed for NJ. It consisted of ABA, sensory integration, speech, Mayer Johnson cards (NJ was hyperlexic), music therapy, and TEACCH in his school. NJ made great progress and spoke his first words at 41/2 years of age following intensive speech therapy. At age 5 he had a streptococcal infection and regressed. It took a year to recover his lost progress. He frequently had sinus infections and ran fevers of 104-105 degrees.

By age 7 he was unable to develop a fever. Fever stimulates the immune system to respond to invaders and creates an inhospitable environment for microbes. He continued to progress until age 9 when NJ got a Strep infection that went undiagnosed for 6 weeks. During this time he developed a severe tic involving his head and neck. He started to tantrum. His Anti-Streptolysin O (ASO) antibody level was 400: normal range is <100. He was treated with Augmentin for 10 days and referred to a neurologist who diagnosed PANDAS. He was started on clonidine for the tic and prophylactic penicillin. This helped, but his gains were greatly impaired. His Mom observed that when he became ill, instead of getting a fever his tic flared and his behavior deteriorated. This made it hard for him to stay in school. NJ continued to have frequent sinus infections which were treated with antibiotics and occasional steroids, but if his dose was even 1 hour late, his symptoms would return, requiring more days of treatment.

In 2007 NJ was 12 and in the sixth grade. Mom was becoming more concerned that “. . . the PANDAS [was] damaging his brain.” She thought, “If I can find a way to get NJ’s immune system to start protecting his brain, I know he will make a tremendous recovery.” His mom convinced his teachers to keep him mainstreamed. At that time, NJ weighed 200 lbs and was on a .01 mg clonidine patch, 15 mg of Lexapro, and 25 mg of Straterra. His tic and behaviors were a major problem and he was obsessive. He was cursing at school and eating lunch in the principal’s office. The PANDAS illness was being managed on penicillin. NJ was switched to erythromycin because he developed erythema multiforma while on the penicillin. His sinus infections persisted and were debilitating. NJ was on Zithromax every other month to treat them. Notwithstanding, he had not run a fever in 6 years.

That summer NJ’s dentist reported 4 impacted wisdom teeth and an impacted canine tooth. Post-op NJ suffered recurrent surgical infections in all five sites. He was not able to handle his own mouth flora. He was treated with two rounds of Zithromax and one round of clindamycin for the ensuing cellulitis. By October, the infection was seated in the hard palate and the cellulitis was raging. NJ’s face was swollen, and he was still in pain. He had a positive nasal culture for methicillin-resistant Staphlococcus aureus (MRSA). These were treated with Bactrim and clindamycin. There is no evidence of infection on his white blood cell (WBC) profile. His ASO was <100, which

is normal. He was still unable to run a fever and his C-reactive protein was <0.1. C-reactive protein is a marker for inflammation.

NJ was referred to a research immunologist to rule out a CD19 deletion (Sinichi, Hasegawa, Fujimoto, Tedder, Takehara, 2000). He was diagnosed with an undescribed PI disease CD19 deficiency. His CD19 level was 4; the normal value is 6-19 (see figure 4). The specialist explained that NJ showed no immune memory of a Strep infection. He could make antibodies but they “didn’t stick to their targets very well, and in the case of Strep, to the bacteria that causes the illness.” In that moment, Mom had an explanation for what had been happening to him for all of those years: his immune system could make antibodies to disease-causing organisms but the antibodies could not reach their targets and destroy them due to the faulty CD19 signaling system. NJ was defenseless.

The treatment plan was to challenge his B cells to produce antibodies using the super pneumoccoccal vaccine. After receiving the vaccine, his B cells produced antibodies (see figure 5). This was the lab test that ruled out the CD19 deletion and suggested the undescribed CD19 deficiency. A “watch and wait” approach was advised.

Post-vaccine, NJ deteriorated. The cellulitis in his face worsened. His WBC counts did not respond to the infection in his face. Antibiotics were given on a more frequent schedule because they offered some relief from the cellulitis. NJ had a team of 10 doctors, including his immunologist since age three. Mom was concerned that NJ was going to die. She brought NJ to a functional medicine doctor, and he recommended a magnesium chloride challenge over 24 hours. NJ started to turn around, and then he stabilized.

Mom was referred for TF by NJ’s functional medicine doctor. We began TF with the blessings of his long-time (since age three) and trusted immunologist, Dr. W. It was February 2008, and NJ was 13 years old. His baseline ATEC was 29. He began to improve weekly. In March, he had a cold laser treatment on his palate where the bone infection was. The laser treatment was to promote healing. By May 2008, NJ was successfully weaned off antibiotics! He had been on TF for 10 weeks. Dr. W. offered the option to discontinue erythromycin prophylaxis for PANDAS and Mom accepted. NJ continued to improve weekly. By the start of the 2008 school year, he had been weaned off Straterra and clonidine. He was sleeping well, and his behavior was improved. By the end of the school year, he was off all medication. Dr. W. reported that NJ’s B-cell CD19 marker was 25.5 and his CD4/CD8 ratio was 1.8. He had rechecked NJ’s lab results seven times. It was unbelievable. Since NJ only had one pneumococcal vaccine, he states that it must be the immune regulating benefits of the TF, but he couldn’t prove it. NJ’s immune profiles look essentially normal.

During the first year on TF, NJ’s nonverbal IQ

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By age 7 he was unable to develop a fever. Fever stimulates the immune system to respond to invaders and creates an inhospitable environment for microbes.

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Figure 4: NJ’s Immune panel before and after TF. NR=Normal Range.*CD4 = mature T helper cells; CD8 = mature antigen specific cytotoxic T lymphocytes. Post TF correlates with CD19 B cell receptor site functionality and CD4/CD8 are with in normal range.

Test 11/7/07 prior to TF 5/7/09 10 weeks post TF

CD4/CD8 ratio 5.62 1.8 NR 1-3.5 NR 1.00-3.90

CD19 absolute 0.089 816 NR 0.070-0.910 NR 65-980

CD19 % 4.0 25.5 NR 6-19 NR 5.4-22.7

*Note: column 2 & 3 normal ranges are different due to testing having been done at different facilities.

Figure 5. S.pneumoniae Antibodies titer challenge results. Note that the first and only pneumoccoccal vaccine was given October 2007. NJ’s titers respond and rule out a true CD19 deletion; instead he has a CD19 defect. A deletion is a genetic defect and would have been reflected in no rise in antibody titer but an extremely high rise in auto antibodies; a defect shows a rise but the antibodies do not adhere to the targeted microrganism. CD 19 deletion is an example of autoimmunity, when the immune cells produce auto antibodies or antibodies against self. CD 19 defect is not described in the immunology literature, but it has been noted. In NJ’s case. His B cells make antibodies but they do not adhere to their viral and bacterial targets, which would otherwise mark them for destruction. TF was started after NJ’s February 2008 labs; by June, antibody production is looking more regulated. Eighteen months later he still has antibodies suggesting to his immunologist that his CD19 defect has been corrected in correlation with TF use.

S.pneumonia Antibodies 9/25/07 11/28/07* 2/4/08 6/24/08 5/20/09Pneu Serotype 1 IgGMedian 2.0 0.9 9.1 9.9 5.9 4.8Pneu Serotyoe 3 IgGMedian 2.2 0.3 1.0 0.8 0.4 0.3Pneu Serotype 4IgGMedian 1.1 <0.2 3.2 2.3 1.4 1.1Pneu Serotype 6B IgGMedian 4.1 1.5 17.2 19.5 14.0 9.8Pneu Serotype 7F IgGMedian 6.2 0.9 1.1 1.6 1.3 2.3Pneu Serotype 8 IgGMedian 4.1 1.1 4.9 5.2 2.2 1.9Pneu Serotype 9N IgGMedian3.7 0.6 8.8 10.3 6.8 6.2Pneu Serotype 12F IgGMedian1.2 <0.1 <0.1 <0.1 0.4 0.3Pneu Serotype 14 IgGMedian 6.7 0.5 4.3 3.7 2.0 1.7Pneu Serotype 18C IgGMedian 1.1 0.6 1.1 1.2 1.5 0.7Pneu Serotype 19F IgGMedian 3.7 2.9 7.3 4.6 5.3 5.4Pneu Serotype 23F IgGMedian 13.1 1.8 1.5 2.0 1.5 3.0Pneu Serotype 5 IgGMedian 8.8 <0.60 1.40 3.00 3.3 2.7Pneu Serotype 9V IgGMedian 11.5 3.20 4.10 1.90 1.3 1.2

Above: Nov 2005 NJ in his in ice hockey uniform.

scores rose by 10 points. He had only been to the principal’s office once and ate with the other kids in the cafeteria. His tic was absent.

By year 2, NJ’s ATEC score dropped to 12. His guidance counselor told Mom that her son was a “very polite young man.” He’d had a teaching assistant since age 4; she was to be released for the school year beginning 2010. NJ started playing the drums and was in the school play. He sang in the Christmas concert. NJ got a life outside of autism. He remains on stress doses of the TF. Medical monitoring will be needed to determine how long NJ will need TF for immune regulation.

DiscussionThese case reports are predicated on the science that came before. It is known that TF is recognized by the immune system as “self.” In my experience, TF is dose dependent. The dose is determined by the recipient’s lack of immune competence, not by age or weight. Dose regimens are adjusted to the individual using clinical parameters. The selection of a TF product depends on the recipient’s tolerance to ingredients. TF is nontoxic to the body.These cases demonstrate correlating clinical benefit using the ATEC, and in NJ’s case immunological laboratory findings. In the first case, a toddler’s near normal ATEC correlates with a protocol of TF. PA struggled to make progress in his in home ABA program for 18 months. Supplementing with dietary TF correlated with PA meeting and exceeding his developmental and cognitive milestones during the first 20 weeks of use. In NJ’s case of ASD complicated by PANDAS and CD19 defect, his immune studies are essentially normal after using TF for 15 months. His daily

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life improved over the first 10 weeks of TF use. It is unusual to have access to immune studies, so I encourage families to track progress using the ATEC. While this may be an imprecise gauge of immune function, it is a pragmatic approach to accessing immune challenge as expressed in behavior, health, sensory integration, and communication. These are the areas of

functioning assessed by the ATEC. A balanced immune response is critical to good health, and the ability to induce one from exogenous TF is suggested here. It is my hope that immune modulation with TF is recognized as safe and effective in children who contend with autoimmunity in ASD and that independent research in this area is pursued.

Ashwood P, Anthony A, Pellicer AA, Torrente F, Walker-Smith JA, Wakefield AJ, (2003). Intestinal lymphocyte populations in children with regressive autism:evidence for extensive mucosal immunopathology. Journal of Clinical Immunology. Nov;23(6):504-17.

Ashwood P, Anthony A, Torrente F, Wakefield AJ. (2004). Spontaneous mucosal lymphocyte cytokine profiles in children with autism and gastrointestinal symptoms: mucosal immune activation and reduced counter regulatory interlukin-10 (2004). Journal of Clinical Immunology. Nov;24(6):664-73.

Bennett RH, Vaughn BM, Lefler SM, McCausland CW, Lisonbee D. (2009). Salivary IgA in healthy adults is increased by dietary transfer factors: an open label cross over study. Manuscript submitted for publication.

Bock, K, (2004) Transfer Factor: immune system modulators. Autism-Aspergers Digest. May-June:32-35.

Corthe’sy B.(2007). Roundtrip ticket for secretory IgA: Role in mucosal homeostasis? The Journal of Immunology, 178:27-32.

Dwyer, JM. (1996) Transfer Factors in an age of molecular biology: A review. Biotherapy. (9)7-11.

France GL, Marmer DJ, Steele RW. (1980). Transfer Factors from human breast milk and breast milk lymphocytes. Clinical Research. 28(5):863A.

Gupta S, Aggarwal S, Rashanavan B, Lee T. (2005). TH1 and TH2 like cytokines in CD4+ and CD8+ T cells in autism. Journal of Neuroimmunology. 85(1)106-109.

Imai K., Matsuyama S, Miyake S, Suga K, Nakachi K. (2000). Natural cytotoxic activity of peripheral-blood lymphocytes and cancer incidence: 11 year follow up study of a general population. The Lancet. 356:1795-1798.

Kidd P. (2003). Th1/Th2 Balance: The hypothesis, its limitations, and implications for health and disease. Alternative Medicine Review. 8(3): 223-246.

Kirkpatrick CH. (2000). Transfer Factors Identification of conserved sequences in transfer factor molecules. Molecular Medicine. 6(4):332-341.

Kirkpatrick CH, Hamad AR, Morton L. (1995). Murine transfer factor:Dose-relationships and routes of administration. Cellular Immunology. (164): 203-206.

Kisielevsky MV, Khalyurina EO, Vorobiev A. (2005). Effects of dietary transfer

factor advanced formulas containing E-EF blends on natural killer (NK) cell activity. Russian Cancer Research Center, Russian Academy of Medical Sciences, Moscow, Russia.

Lang I. (1982). Effect of in vivo and in vitro treatment with dialyzable leukocyte extracts on human natural killer cell activity. Clinical Immunology and Immunopathology. 25:139-144.

Lawrence HS. (1949). The cellular transfer of cutaneous hypersensitivity to tuberculin in man. Proc Soc Exp Biol Med. (71): 516.

Paremly MJ, Beer AE. (1976). Colostral cell-mediated immunity and the concept of a common secretory immune system. Journal of Dairy Science. 60(4):655-665.

PizzaG, DeVinci,C ,Fornarola V, Palareti A, Baricirdi O,Viza D. (1996). In vitro studies during long term oral administration of specific transfer factors. Biotherapy. 9(1-3):175-185.

See, DM, Khemka P, Sahl L, Bui T, Tilles JG. (1997). The role of natursl killer cells in viral infections. The Scandinavian Journal of Immunology. (46):217-224.

Sinichi S, Hasegawa M, Fujimoto M, Tedder TF, Takehara K. (2000).

Quantitiative genetic variation in CD19 expression correlates with autoimmunity. The Journal of Immunology. (165): 6635-6643.

SinghVK. (2009). Phenotypic expression of autoimmune autistic disorder (AAD) a major subset of autism. Annals of Clinical Psychiatry. 21(3):148-161.

Singh VK. (2005). Elevated serum C-reactive protein and S100 protein for systemic inflammation in autistic children. Journal of Special Edication and rehabilitation. (3-4):117-25.

Singh VK, Jensen RL. (2003). Elevated levels of measles antibodies in children with autism. Pediatric Neurology. Apr;28(4):292-4.

Singh VK, Warren R, Averett R, Ghaziuddin M. (1997). Circulating autoantibodies to neuronal and glial filament proteins in autism. Pediatric Neurology. 17(1):88-90.

Wilson G, Paddock G. (1983). United States Patent 4 816 563.

Vorobiev AA. (2004). Transfer Factors use in immunorehabilitation after infectious-inflammatory and somatic disease, Ministry of Health and Social Development of the Russian Federation, Moscow, Russia.. Methodological Letter.

References

Above: Nov 2009, NJ in his suit.

Interval Total Speech/Lang/Comm Sociability Sensory/Cognitive Awareness Health/Physical/behavior

Baseline 29 4 6 5 14

2 year 12 4 1 2 5

Figure 6: NJ’s ATEC changes with TF supplementation.

I want to extend a special thank you to Michelle and Susan and their incredible husbands and families for allowing me to tell your stories. May your intuition and trust in your children’s ability to heal inspire others. I would also like to extend my appreciation to Richard Bennett, PhD, for his expertise in immunology and the daunting task of teaching immune system science.

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