The Lyme-Autism Connectionby Tami Duncan

Does Lyme Disease Cause Autism?Proving Congenital Transmission

In case you hadn't heard yet, autism spectrum disorderis now said to affect one out of 150 children in the UnitedStates alone. These numbers only include autism diagnosisand don't take into account the increased numbers ofPersuasive Developmental Disorder - Not OtherwiseSpecified (PDD-NOS) or Asperger's Syndrome, which arealso considered on the broad spectrum of autism. Obsceneamounts of thimerosol injected into babies can be blamedfor triggering autistic symptoms in many of these children,but what can explain the susceptibility factor? Why did mychild get autism and your child didn't? Furthermore, whywould a family's first child, who was vaccinated, get autismand subsequent non-vaccinated siblings also developautism? The answer could lie with the mothers.

With the increasing numbers of chronic illnesses in oursociety today, one can even refer to this phenomenon as aworldwide epidemic, a disease society. Children are sickwith food allergies, childhood diabetes, and asthma, toname a few conditions. They are neurologically affectedwith autism, Asperger's syndrome, PDD-NOS, bipolardisorder, ADHD, depression, and obsessive compulsivedisorder. Adults are ill with multiple sclerosis, fibromyalgia,chronic fatigue syndrome, diabetes, cancers, allergies,intolerances, celiac disease, and the list goes on. Wemust open minds to causes other than just vaccines, whenconsidering the complete state of health of this country. Weare living in sick bodies in a toxic world. If we can solvethis autism puzzle, then we have a chance of changing thisdiseased society in which we live.

Infections may be the answer we need to solve thispuzzle. The multiple infections that we all have in commonneed to be looked at. A compromised immune system isallowing these microbes to have a field day on our bodies.

When looking at infections, one cannot ignore the manytick-borne diseases such as Borrelia, Mycoplasma, andBartonella, which are rampant in our population today.

"How could my child have Lyme disease?" This is themost commonly asked question among parents who havea child affected by autism. When a child with autismcomes back with a positive lab result for Borrelia, parentsask themselves, how could this be? I often hear parentssay, "My child has never had a tick bite." Physicians needto be armed with information to educate parents on theharsh reality of what may be contributing to this autismepidemic.

Lyme disease has been known as the great imitator.'Its ability to mimic the symptoms of chronic fatigue,fibromyalgia, and multiple sclerosis,^ among others, isnotorious. Many people have received these diagnoses, butwhen a keen physician probes further, they find that many,in fact, have Lyme disease. This is a common phenomenonwith mothers of autistic children. Many mothers themselvesare not well. When asked, most mothers will tell you thatthey have fibromyalgia or chronic fatigue syndrome or, atthe very least, food allergies, fatigue, and general malaise.Usually, mothers ignore their symptoms, feeling that theymust just be tired because they are overwhelmed fromthe demands of having a child with special needs. Manymothers ignore their own treatment, feeling that they needto focus alt of their resources on their child.

New Evidence Could Point to Congenital TransmissionA new study from the University of California, Davis

may have stumbled upon new evidence regarding therelationship between a mother's health and the diagnosisof autism in her child. Recently, in Neurotoxicology, a

68 TOWNSEND LETTER - JUNE 2008

study by D. Braunschweig et al., titled "Autism: Maternally-Derived Antibodies Specific for Fetal Brain Proteins,"'determined that "the presence of maternal autoantibodiesto fetal brain proteins of approximately 37kDa and 73kDamolecular weight confers an elevated risk for autism."The authors state that "these data provide evidence foran association between the presence of maternal immunesystem biomarkers and a diagnosis of autism in a subsetof children. The presence of specific anti-fetal antibodiesin the circulation of mothers during pregnancy maybe a potential trigger that, when paired with geneticsusceptibility, is sufficient to induce a downstream effecton neurodevelopment leading to autism."

So what are these antibodies that are attacking the fetus'brain? Robert Bransfield, MD, of Red Bank, New jersey,provided information for the LIA Foundation's'' East CoastConference in April on just what this may mean, it may beone more link connecting Lyme disease to autism and is oneof several possible processes that may explain how Borreliaburgdorferi infections can result in autism. Bransfield statedthat from his research he found that 37kDa is associatedwith Neuroborreliosis,^"^ E.coli,'* Bartonella,'" andMycoplasma."'^ 73kDa is found in chlamydia,''' strep,''Mycoplasma,'^ Bartonella,'^ and Borrelia burgdorferi.^'^He also put the numbers together to show that in the 37children tested, 37kDa was found in 28% of regressiveonset autism cases and 21% of early onset autism cases,'**which is similar to what the current research is showingfor incidence of Lyme in autistic children, reported at a20-30% incidence.^" Therefore, showing that bands 37 and73 are both found in Borrelia burgdorferi and as maternallyderived antibodies now known to cause autism showsevidence of congenital transmission.^'

In Bransfields' research compilation, he discoveredthat two other tick-bornediseases appeared to bejust as concerning asBorrelia: Mycoplasma andBartonella. This increasessuspicion as to thepresence of a tick-bornecause. It is already provenfrom Professor GarthNicolson of the Institutefor Molecular Medicinethat Mycoplasma is foundin 587o of the childrenwith autism spectrumdisorder." Tick-bornediseases in generalshould be a concern forcongenital transmission inlight of this new evidence.It is important to note thatonly tic-borne diseaseshold in common bothbands 37kDa and 73kDa.

Now that Bransfield has put the science together, didthis LJC Davis study contribute to the proof that congenitaltransmission of Borrelia burgdorferi and/or tick-bornedisease can cause autism? Before stating this with certainty,more research needs to be done in this area to prove thishypothesis. However, it should give physicians and parentsof autistic children suspicion that this could in fact be areality for many children on the spectrum.

Autism Prevention - Cutting Off the Epidemic at ItsKnees!

This study shows the desperate need for an autismprevention program. Testing young women for theseinfections before they conceive is imperative and providingproper treatment to minimize transmission to the fetusis essential. What if half of the autism cases could beprevented?

Science has not proven any concrete cause for mostchildren with autism, but subsets of children exist, creatingmany "autisms," or categories of children with autism thatare different from each other. The Lyme-Autism connectioncurrently appears to affect 20-30% of children withautism spectrum disorder.^' This is a large enough subsetthat potentially could be prevented if young mothers areeducated on proper health, testing for heavy metals, andidentifying infections prior to conceiving. The authorencourages e-mails from interested physicians who wouldlike to assist in creating an autism-prevention program.

Long ago, the refrigerator mother myth was debunked,thanks to Bernard Rimland of the Autism ResearchInstitute^^ in San Diego, California who discovered themedical realities that autistic children exhibit. However,many mothers still place a heavy weight of self-inflicted

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The Lyme-Autism Connection 5.

guilt upon themselves, wondering if they did something tocause this in their children, tt is unrealistic to think that anymother u'ould knowingly do anything to hurt their unbornbaby. Do not misunderstand the intentions of this article.Knowledge is power. We can only begin to heal ourchildren if we open our minds to all possibilities, examinethe science, and take a stand to prevent further cases whilehelping our precious children today.

Tami DuncanPresident of LIA FoundationWebsite: www.liafoundation.orgE-mail; Tami@liafoundation.org

Notes1. Pachner A. Neurologic manifestations of Lyme disease, the new "great

imitator." Rev Infect Dis. 1989 Sep-Oct;l 1 Suppi 6:S1482-6.2. Nicolson G. Systemic intracellular bacterial infections in

neurodegenerative and behavioral disorders. Infectious DiseaseNewsletter. 2007.

3. Braunschweig D, et al. Autism: Maternally derived antibodies specificfor fetal brain proteins. Neurotoxicology. 2007.

4. For more information, please visit the [Lyme-induced Autism] LIAFoundation at www.liafoundation.org.

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2CX)8 Cormrtlon.Conlinmcr

Thursday, June 26th

Friday, June 27th

Saturday, June 28th

Sunday, June 29th

Physician's Training

General Session and Dinner Event

General Session

Tee Up For Autism Charity Golf Toumament

General Session

This 2008 conference will feature top speakers in the field of Lyme disease, autism and

alternative medicine. Learn from the best such as;

Steven Harris, M.D., Lee Cowden, M.D., Garry Gordon, M.D., Aristo Vojdani, PhD, Stephen

Buhner author of "Healing Lyme", Jeff Wulfman, M.D., Leo Shea, PhD, Judith Leventhal,

PhD, Amy Derkesen, ND, Tamara Mariea, CCN, Christie Dames, Brooke Landau, Nicola

McFadzean, N.D., Allan Sosin, M.D., Richard Horowitz, M.D., Cindy Griffin, Jeff Baker.

N.D., Toby Watkinson, DC and Deitrich Klinghardt, M.D. ,

Cinco M, Murgia R, Ruscio M, Andriolo B. IGM and IgG significantreactivity to Borrelia burgdoreferi sensu strict, Borrelia garinii andBorrelia afzelii among Italian patients affected by Lyme arthritis orneuroborreliosis. Immunol Med Microbiol. 1996|un;14(2-3): 159-66.Cilmore RD |r, Murphree RL, lames AM, Sullivan SA, lohnson B|. TheBorrelia burgdorferi 37-kilodalton immunoblot band (P37) used inserodiangosis of early lyme disease is the flaA gene product. I ClinMicrobiol. 1999Mar;37(3): 548-52.Feng S, Hodzic E, Barthold SW. Lyme arthritis resolution withantiserum to a 37-kilodalton Borretia burgdorferi protein. Immun.2000 |ul;68(7):4168-73.Sala7ar CA, Rothemich M, Droin EE, Glirkstein L, Steere AC. HumanLyme arthritis and the immunoglobulin G antilx)dy response to the37-kilodalton arthritis-related protein of Borrelia burgdorferi. InfeclImmun. 2005 May;73(5):2951-7.Ohshima T, Nunoura-Kominato N, Kudome T, Sakuraba H. Anovel hyperthermophilic archaeal glyoxylate reductase fromThermococcus litoralis. Characterization, gene cloning, nucleotidesequence and expression in Escberichia coli. Eur I Biochem. 2001Sep;268(1 71:4740-7.

10. Haimerl M, Tenter AM, Simon K, Rommel M, Hilger J, AutenreithIB. Seroprevelence of Bartonella henselae in cats in Germany. / MedMicrobiol. 1999 Sep;48(9): 849-56.

11. Fleury B, et al. Characterization of P40, a cytadhesin of Mycoplasmaagalactiae. Infect Immun. 2002 Oct;70(10):5612-21.

12. Gorton TS, et al. Antibody-mediated selection of a Mycoplasmagallisepticum phenotype expressing variable proteins. FBMS MicrobiolLett. 1997Oct1;155(1):31-8.

13. Hasebe A, et al. Inflammatory lipoproteins purified from a toxigenirand arthritogenic strain of Mycoplasma arthritidis are dependent onToll-like receptor 2 and CD14. Infect Immun. 2007 Apr;75(4):1820-6.

14. KanamotoY,etal.,Antigenic characterization of Chlamydia pneumoniaisolated in Hiroshima, Japan. Microbiol Immunol. 1993;37(6): 495-8.

15.Choi IH, et al. Limited stress responsein Streptococcus pneumonia. MicrobiolImmunol. 1999;43(8):807-12.

16.Degiorgis MP, et al. Immune responsesto Mycoplasma coniunctivae in alpineibex, alpine chamois, and domesticsheep in Switzerland. / Witdl Dis. 2000Apr;36(2):265-71.

17.Haimerl M, et al. Seroprevalence ofBartonella henselae in cats in Germany. /Med Microbiol. 1999 Sep;48(9):849-56.

18.Luft BJ, et al. Immunologic and structuralcharacterization of the dominant 66-to73-kDa antigens of Borrelia burgdorferi. IImmunol. 1991 April 1 5;146(8):2776-82.

19. Braunschweig D, et al. Autism: Maternallyderived antibodies specific for fetal brainproteins. Neuroloxico/ogy. 2007.

20.Bransfield RC, et al. The associationbetween tick-borne infections. MedHypotheses. 2007.

21.Bransfield RC. Information provided forLIA Foundation 2008 conference, April 12,2008. Fort Lee, New Jersey.

22. Nicolson G. Systemic intracellular bacterialinfections in neurodegenerative andbehavioral disorders. Infectious DiseaseNewsletter. 2007.

23.Bransfield RC, et al. Op cit.24. Autism Research Institute. Available at:

www.autism.com. .

Where: Hyatt Grand Champions ResortandSpa in

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70 TOWNSEND LETTER - JUNE 2008