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The cause of some autism cases may be from an infectious agent which can include Lyme disease.

As more research is done the more compelling this argument becomes. We attempt here to centralize some of the data.


From: http://www.bio-medicine.org/medicine-news/Antibiotics-Helps-Autism-28-1/

There is new hope for children with autism. Antibiotcs seem to treat or prevent the symptoms of autism in some patients.

One in every 150 children is affected by autism. Currently there are no treatments for this complex condition. Researchers from Rush-Presbyterian-St. Luke's Hospital in Chicago found that a subset of patients with autism who experience a colonization of bacteria in the bowel can be helped by antibiotic vancomycin.

Interestingly the study was done after the autistic son of a researcher was treated with antibiotics for an ear problem and showed improvement of his symptoms. Researchers at present are not sure why the therapy works, they hypothesize that it may be that the symptoms of autism are caused by a neurotoxin-producing bacteria (a bacteria that inhibits the function of cells in the nervous system). However there are still many questions to be answered about this complex condtion.

AUTISM-A TYPE OF LYME DISEASE


Medical Hypothosis
Kathy Blanco
December 15, 2004
Copywrite 2004

Autism is growing at epidemic rates. (1) It is reported to be prevelant in
1-150 children, some states 1-80 children. Autism is a complex neurological
disorder with seemingly provable and many etiologies such as maternal viruses
and bacteria (2), immediate cord clamping and birth drugs (3), metabolic
insufficiency during development in utero or infancy (ie, thyroid t3 and t4)
(4), purine disorders, adenosine deaminse deficiency (5), mitochondrial
disorders (6), iron fragile metabolism (7), metallothionein deficiency (8),
oxidative stress, childhood vaccinations which act as triggers to events above
through viral persistance in gut and brain (9), and heavy metal poisoning from
additives in vaccines (10), and lastly chronic disseminated lyme
neuroborreliosis disease. Lyme disease is transmitted through a tick bite. But
it can also be transmitted through semen, breast milk and gestational fluids.
This means that a fetus can be infected by its mother. B. burgdorferi has been
proven by PCR analysis to establish a persistent infection in the mammalian host
(Straubinger, R. Persistence of B. burgdorferi in experimentally infected dogs
after antibiotic treatment. J.Clin.Microbiol.1997 Jan; 35(l): 111-116).
Lyme disease is the fastest growing vector-borne disease in the nation. In 2001,
the Center for Disease Control recorded 18,000 new cases, but some experts
estimate that the actual number is closer to 200,000. This is four times the
number of HIV cases per year. Autism grows as exponetially as that, and an NIH
bulliten explained of late it is seen in 1/166 children. Amongst those
statistics, is the further frightening 1-6 children now have a developmental,
psychiatric problems in the US.
Lyme disease results in underconnectivity of brain areas, defects of the
fusiform gyrus and loss of purkinje cells in the cerebellum. Recently reports
of white matter disease are prevelant in children and adults with autism
paralleling patterns in lyme disease. (11) Late in the progression of this
disease neurological, cognitive, and psychiatric symptoms predominate,
overlapping symptoms of autism, such as food avoidance, facial recognition
problems, sleep disorders, ocular symtpoms such as light sensitivity, speech and
language loss or word retrieval problems, noise sensitivity, bed wetting,
aggression, panic attacks, headaches, movement disorders, sore throats and poor
swallowing, hypofusion-poor blood flow particularly to temporal lobes, swollen
tongues and lymphs, chronic fatigue symptoms, hyperactivity, gut problems (ie,
diahrreah, constiptation, IBD symtpoms, Celiac symptoms), liver dysfunction,
thyroid problems (t3 and t4 conversions), iron disorders, heavy metal toxicity,
tics, food sensitivities, depression, serotonin uptake problems, autoimmune
brain antibodies, problems with sequencing, problems with sensory perceptions,
seizures, cardiac conduction abnormalities, illiod hyperplasia, heavy metal
toxicity, co infections of HHV6 and Mycoplasma (12), various aches and pains
masked as lyme arthritis particularly in the neck area, and zinc copper iron
imbalances.
The basic hierarchy is pre-frontal cortex, para limbic association areas, limbic
structures, and brain stems - hypothalamus. Lyme encephalopathy can result in
dysfunction of the modulation centers, inhibitory pathways, and stimulatory
pathways. (13) Autopsies, animal studies, and brain imaging tests have
contributed to this understanding. The presenting symptoms of NPLD are sometimes
emotional in nature, and include obsessive-compulsive disorder, depression, and
aggression, panic disorder, and other phobic disorders. These self same
observations are also seen in autism as reports from parents of these symptoms
are typical.
All involved with late state Lyme disease agree there is a large amount of
inaccurate information on this subject. This disagreement exists at every level
- journals, scientific meetings, clinical practice, and media outlets. The same
can be said of autism, in which denials of it's etiologies are profusely
displayed as only genetic, and never any environmental iaotragenic factors
involved. Profusely are denials of the existance that autism is based on the
bodies response to a foreign material either of neurotoxicity, bacteria or
virus, such as lyme, such as vaccinal viruses, such as autoimmune processes
that become overabundant. Reports are clear, that parents of autistic children
seem to have higher incidences of autoimmune conditions. This is telling us
something. It is my belief, this is a sign that the parents themselves have
lyme disease-and are giving this infection to their children. Lyme disease is
prevelant in all fifty states of the union, and know no geographical areas.
However, it is interesting to note, that in states that have the less lyme,
there is more availability of selenium in the soils, which is a immune neuro
protectant against viruses and bacteria. Parents of autistic children
routinely show low levels of selenium in blood work, as well as metallothionein
deficiency, a glutathione dependent oxidant. Parents also have higher
sedimentation rates (ESR) and thrombaphilia and fibrin deposits showing
inflammation as well as thyroid TRH dysfunction. (14) They also often have
skewed hormonal balances. Lyme is capable of changing these aspects on blood
work.
Interestingly, susceptibility genes for autism parallel the susceptibility genes
for arthritis and other autoimmune disorders, such as HLA-B27, and HLA-DR4.
Complement immune deficiencies are common in both diseases, including C4B and
C3A. The frequency of autoimmune disorders was significantly higher in
families of the PDD probands compared with families of both the autoimmune and
healthy control probands. Autoimmunity was highest among the parents of PDD
probands compared with parents of the healthy control subjects.
Hypothyroidism/Hashimoto’s thyroiditis and rheumatic fever were significantly
more common in families with PDD probands than in the healthy control families.
Interestingly, reports of Hashimotos and hypothyroidism are prevalent in lyme
disease. (15) Interestingly, reports of mycoplasma are consistent with parents
having a mycoplasmal infection, and giving that to their children. (16)
Mycoplasma medications are alleviated by the self same medications for lyme
disease. Many parents report that lyme and mycoplasma are prevelant in their
children with autism. Familial association studies have also reported an
increased risk of several systemic autoimmune diseases among relatives of
patients with a systemic autoimmune disease. This association may reflect a
common etiologic pathway with shared genetic or environmental influences among
these diseases. Environmentally, there is increases in levels of heavy metals,
toxicity, neurotoxicants, mold, and most of all but not least, the prevelance of
the lyme bacterium. Prolactin may also have important immune-modulating
influences affecting the risk of autoimmune disease . The prolactin gene is
located close to the MHC region of chromosome 6, hotspots for lyme AND autism.
(17) Another protein eaten by lyme is melatonin, which may account for levels
of serotonin, prolactin and the ability to detox heavy metals. In autism,
melatonin levels are dysregulated, causing sleep disorders, and antibodies are
found against serotonin.
Recently there have been reports of short term antibiotic use to kill
clostridium and or AGBN's. Vancomycin was recently used, and reports are that
when on the antibiotic for thirty days, symptoms of autism decreased. The
Jarish Herxheimer reaction is seen when antibiotics are having a therapeutic
effect as well, as evidenced when the child is on the antibiotics. This often
scares off the weary parent of an autistic child, stopping the antibiotic for
fear it is contributing to their autism symptoms when in reality it was killing
lyme with mild to moderate reactions. Unfortunately, in these studies, the
children regressed back to autism symptoms as soon as they were removed after
thirty days. If the bacteria is not completely eliminated, the symptoms will
return. This tells us, I believe, that lyme is involved in their autism. This
reasoning has made others think of why these children respond so favorably while
on the antibiotic. It could be that it is going after the lyme bacterium
(however not it's stages due to it's short length), but also calming down the
cytokine and chemokine activity in the immune system, and having some kind of
effect on viruses which depend on cytokines and chemokines. Typically those
viruses are of the herpes CMV class. Reports of HHV6 and autism are abundant.
Many children have high herpes titres, sometimes to that of 4-6 times of normal,
often corrolating with autism symptoms or seizures. Although the American
Academy of Pediatrics recommends a three week course of antibiotics, Dr. Jones-a
pediatric lyme speclialist, has found that the bacteria that causes Lyme has
become increasingly hardy and even when the disease is caught early, it often
needs to be treated with an eight to twelve week course of antibiotics or
beyond.
Lyme has many names. Among its "symptoms" are ALL of the "ideopathic"
(unknown-cause) diseases that plague americans, too many to list here - it
affects the body by making sugar turn to lactic acid, which in turn can scar the
kidneys over time, irritate the bladder, damage the liver, and upset the
pancreas. Lactic acid causes muscle soreness and sensitive intestines/cramping
problems (nervous stomach). Interestingly, it is reported that many autistic
children have skewed lactic and pyruvate ratios. This creates a mitochondrial
disorder, oxidative stress in these children. Lyme also eats proteins, many
types. It eats myelin protein, which is known to be going missing in MS
patients. The
localities for MS hot spots exactly match the pattern of lyme disease, and I
believe it is the same disease with a different name. Myelin is what nerves are
made of - and damage to myelin, without a meat and potatos diet to replace
protein constantly, causes brain troubles (alzheimers, parkinsons, alateral
myotrophic scleroses, myocarditis), numbness of the bladder and/or muscle spasms
in the elderly mistaken as "incontinence", nerve troubles, stuttering, etc.
This corrolates nicely with what we are seeing in autism. Typically there are
myelination antibodies in children with autism, even Neural Axon Filament
Protein antibodies, and various other antibodies against brain tissue. Many
children with autism lose their ability to sleep through the night without
bedwetting. Stuttering is often seen in children with autism.
It is also reported that when these children harbor heavy metals, that viruses
and bacteria seem to live in areas of that damage. Since these children lack
the oxidant metallothionein, they cannot detox the EPA over standard of safe of
thimerosol that were in childhood vaccine series, or other environmental factors
including their mothers in utero exposure of amalgams. Unfortunately, they
still are according to HAPI, a NPO who just tested mercury free vaccines (ARI
newsletter 2004). As they work in consortium, there is a theory that the
heavy metals bind to these bacteria and viruses, and when they are eliminated,
heavy metals start to chelate out of the body. This is evidenced by EDTA
chelation which has the ability to kill nanobacteria. Observations and
biomarkers of damage are seen soon after vaccinations, but what is equally
intriguing, is that lyme may be awoken after an immune lowering event such as
vaccinations.
Recent reports show that children with autism are harboring lyme disease. The
cry for chromosomal faults are numerous, and often paid and backed to be equally
the only way you get autism. What researchers know, is that no money is funded
or researched or goes into the immune lowering/autoimmunity events that create
autism, and is simply put down. The cogent finding of lyme bacterium being a
major risk factor for autism needs to be explored. This is superimposed on the
already sustained belief, that autism is an autoimmune disorder. Many of the
imbalances of autism could be explained as the body's inability to detox and to
work on this bacteria. Lyme could also be a trigger or a circumstance that
initiate or worsening of the autistic condition. This includes milk allergies,
strep infections, mercury, dietary intolerances of wheat and milks, and
inability to deal with toxic inhibitors. Interestingly, many of the imbalances
and deficiencies can be caused by lyme bacteria.
Many of the meds used for autism seem to also slow down the lyme bacterium, such
as digestive enzymes, anti fungals, of course, antibiotics, anti parasticals,
addressing food allergies, increasing zinc, antiinflammatories and even secretin
(secretin is tied to insulin, which lyme attacks). Lately, the use of
Methylcolbalamine B-12 with folinic acid would also reduce lyme symptoms. Since
there is already evidence of abnormal gut bacteria and exaggerated production of
cytokines which result in irreversable cellular damage, it behooves parents and
clinicians and researchers to look into this paralell and seek state of the art
laboratory connections to lyme and autism. Three labs are recommended,
STONYBROOK, BOWEN and IGENEX. This may result in the first of it's kind
treatment for autism via lyme therapy.
References
(1) Changes in the Population of Persons with Autism and PDD, Dept Develop
Services, California, Health and Human Services March 1 1999
(2) The Journal of Neuroscience, January 1, 2003, 23(1):297-302
Maternal Influenza Infection Causes Marked Behavioral and Pharmacological
Changes in the Offspring
(3) IMFAR-IMMEDIATE CORD CLAMPING and AUTISM, Dr Morley www.cordclamping.com
(4) Abramson J, Stagnaro-Green A. Thyroid antibodies and fetal loss: an
evolving story. Thyroid 2001;11(1):57-63.
(5) Adenosine Deaminase - Neurogenetics. 2001 Mar;3(2):111-3. Related
Articles, Links
Autism: evidence of association with adenosine deaminase genetic polymorphism.
Bottini N, De Luca D, Saccucci P, Fiumara A, Elia M, Porfirio MC, Lucarelli P,
Curatolo P. Department of Internal Medicine, Tor Vergata University of Rome,
Rome, Italy
(6) J Child Neurol. 2000 Jun;15(6):357-61. Related Articles, Links Autism
associated with the mitochondrial DNA G8363A transfer RNA(Lys) mutation. Graf
WD, Marin-Garcia J, Gao HG, Pizzo S, Naviaux RK, Markusic D, Barshop BA,
Courchesne E, Haas RH. Department of Pediatrics, University of Washington,
Seattle, USA.
(7) Arch Dis Child 1997;76:264-267 ( March ) Fragile X, iron, and
neurodevelopmental screening in 8 year old children with mild to moderate
learning difficulties N Corrigan,a M Stewart,a M Scott,b F Feec a North and West
Belfast Community Paediatric Unit, Belfast, Northern Ireland, b Queens
University Belfast Department of Epidemiology and Public Health, Belfast,
Northern Ireland, c Belfast Education and Library Board, Belfast, Northern
Ireland
- And
Life Sci. 2004 Oct 8;75(21):2539-49. Related Articles, Links
Oxidative stress in autism: increased lipid peroxidation and reduced serum
levels of ceruloplasmin and transferrin--the antioxidant proteins. Chauhan A,
Chauhan V, Brown WT, Cohen I. NYS Institute for Basic Research in Developmental
Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314, USA.

(8) - Metallothionein Deficiency - see www.hriptc.org Walsh, W, Monograph:
Metallothionein and Autism". {Pfeiffer Treatment Center, Illinois, Oct 2001,
Over 100 articles referenced.
(9) - Wakefield AJ, A Anthoney et al "Enterocolitis in Children with
Developmental Disorders" Am.J Gastroenterology 95 No 9 (2000) p 2285-2295
(10) A case control study of mercury burden in Autistic children in autistic
spectrum disorders (Journal of American Physicians and Surgeons, Vol 8, No 3, 3
Fall 2003) J Bradstreed, MD, D Geier, J Kartzinel, Md, J Adams PhD, M Geier, MD,
PhD.
(11) Cure Autism Now Foundation, White Matter Disease and Autism, see website
(12) HHV-6 and Autism - Clin Immunol Immunopathol. 1998 Oct;89(1):105-8
Related Articles, Links Serological association of measles virus and human
herpesvirus-6 with brain autoantibodies in autism.
Singh VK, Lin SX, Yang VC. College of Pharmacy, University of Michigan, Ann
Arbor, Michigan, 48109-1065, USA.
(13) Activation of the fusiform gyrus when individuals with autism spectrum
disorder view faces, N Hadjikahmi, RM Joseph, J Synder, CF Chabris, J Clark, S
Steel, L McGrath, M Vangel, I Aharon, E Feczko, GJ Harris, and H Tager-Flusberg,
Neuroimage, Vol 22, No 3 July 2004,
(14) J Neuroimmunol. 2004 Jul;152(1-2):176-82. Related Articles, Links
Autoantibody repertoires to brain tissue in autism nuclear families. Silva SC,
Correia C, Fesel C, Barreto M, Coutinho AM, Marques C, Miguel TS, Ataide A,
Bento C, Borges L, Oliveira G, Vicente AM.
Instituto Gulbenkian de Ciencia, Rua da Quinta Grande 6, 2781-196 Oeiras,
Portugal.
(15) Pediatrics. 2003 Nov;112(5):e420. Related Articles, Links
Increased prevalence of familial autoimmunity in probands with pervasive
developmental disorders.
Sweeten TL, Bowyer SL, Posey DJ, Halberstadt GM, McDougle CJ. Department of
Psychiatry, Indiana University School of Medicine, and James Whitcomb Riley
Hospital for Children Indianapolis 46202-4800, USA.
(16) Chronic Mycoplasmal Infections in Autism Patients
Garth L. Nicolson,1 PhD, Marwan Y. Nasralla,2 PhD, Paul Berns,1 MD and Jeorg
Haier,3 MD, PhD
1 The Institute for Molecular Medicine, Huntington Beach, California, USA,,
2 International Molecular Diagnostics, Inc., Huntington Beach, California, USA,

3 Department of Internal Medicine, and 3Department of Surgery,
Wilhelm-University, Munster, Germany. Correspondence: Prof. Garth L. Nicolson,
Office of the President, The Institute for Molecular Medicine, 15162 Triton
Lane, Huntington Beach, California 92649. Tel: 714-903-2900; Fax: 714-379-2082;
Website: www.immed.org
(17) Am J Med Genet. 1999 Nov 5;87(1):17-22. Related Articles, Links
Subtle overlapping deletions in the terminal region of chromosome 6q24.2-q26:
three cases studied using FISH. Sukumar S, Wang S, Hoang K, Vanchiere CM,
England K, Fick R, Pagon B, Reddy KS.
Cytogenetics Department, Quest Diagnostics Inc., San Juan Capistrano, California

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