Link between autism and vaccines should be investigated

Former Head of NIH Says Link Between Autism & Vaccines Should Be Investigated

By Melanie Phillips

Good to see that the Telegraph of London has picked up on developments I wrote about here in the U.S., where a head of official steam is building behind the perception that there is a troubling relationship between certain childhood vaccines, including MMR (mumps/measles/ rubella), and autistic symptoms and other damage in a subset of particularly vulnerable children. As I have written, this has been prompted by recent U.S. cases in which multiple vaccinations have aggravated an underlying mitochondrial weakness to produce catastrophic effects, leading Dr. Bernardine Healy, the former head of the National Institutes of Health, to tell CBS News:

“I think that the public health officials have been too quick to dismiss the [autism link to vaccination] hypothesis as irrational.”

In addition, the Telegraph reported this: “The vaccine hypothesis was bolstered recently by a five-year study in monkeys who were given the same vaccinations that American children are routinely given. Last week, Dr. Laura Hewitson, a specialist in obstetrics, gynecology and reproductive sciences at the University of Pittsburgh, told the International Meeting for Autism Research in London that in the double-blind placebo-controlled study, 13 vaccinated animals showed increased aggression, impaired cognitive skills and developmental delay. The three unvaccinated animals in the study developed normally.”

“There was a significant difference between the two groups,” said Hewitson. “The vaccinated group had trouble developing reflexes. . . . They also became more insular and more aggressive. There was an increase in aggressive behavior after they had their MMR vaccines, and they stopped exploring their surroundings as much.”

Abnormal brain activity was found in the monkeys, and higher sensitivity to a naturally occurring brain chemical linked to sleeplessness, hallucinations, lack of social skills and a high pain threshold—all symptoms found in children on the autistic spectrum. The monkeys also exhibited abnormalities of the amygdala, the part of the brain which regulates emotions.

“We can’t conclude that vaccines cause autism from this study,” said Hewitson. “What we can conclude is that the vaccinated monkeys showed significant negative behavioral differences before and after the MMR.”

This research, carried out at five U.S. research centers, including The University of California, Washington National Primate Research Center, Seattle, The University of Kentucky and the Thoughtful House Center for Children, Texas (founded by the man at the eye of this storm, Andrew Wakefield) has not yet been published in a peer-reviewed journal. Some suspicious minds may think (however unfairly) that Wakefield’s involvement taints it. And it must be stressed that the other American developments involve certain differences from the British childhood vaccination regime, including multiple jabs in the course of one day and the use of mercury-based preservatives.

Nevertheless, it should be noted that the suspicion gathering momentum in the U.S., that a vaccine schedule including MMR may trigger a catastrophic reaction in both brain and gut among a small proportion of children who are vulnerable, is almost exactly the claim made by Wakefield, now fighting for his professional life before the General Medical Register for making it—in the teeth of a medical establishment in Britain that states categorically there is no truth in it whatsoever.

Melanie Phillips is an acclaimed and controversial columnist for London’s Daily Mail. Educated at Oxford, she won the Orwell Prize for journalism 1996. She is the author of All Must Have Prizes and other books. Her website, which collects many of her essays, is www.melaniephillips.com. Please take a look. This article was edited for length.

What DOES the CDC and Julie Gerberding Really KNOW about "AUTISM" and Paternal Age and Vaccinations?

http://www.mothering.com/interactive/mothering-media/mothering-media.html


From Mothering.com on is the CDC acting in the interest of US citizens or the pharmaceutical industry? Paul Offit,etc.

Lack of normal myelination is involved with neurocognitive developmental orders due to sperm mutations and maybe vaccinations

Also read: http://autism-prevention.blogspot.com/search?q=Alzheimer%27s+and+myelination


Written and overseen by Lewis Mehl-Madrona, M.D., Ph.D.
Program Director, Continuum Center for Health and Healing,Beth Israel Hospital / Albert Einstein School of Medicine

Vaccine Induced Demyelination
Myelination is an essential part of human brain development. Nerves can only conduct pulses of energy efficiently if covered by myelin. Like insulation on an electric wire, the fatty coating of myelin keeps the pulses confined and maintains the integrity of the electrical signal so that it has a high signal-to-noise ratio. When the insulation on a wire is damaged or destroyed, the flow of electrical current may be interrupted and a short-circuit occurs.
Oligodendrocyte cells give white matter its color by manufacturing myelin. If myelin falls into disrepair, nerve axons cease to function, even though they themselves aren't damaged. Protecting oligodendrocytes after brain or spinal cord injury might keep nerve cells intact.
At birth, relatively few pathways have myelin insulation. Myelination in the human brain continues from before birth until at least 20 years of age. Up until the age of 10 or so, vast areas of the cortex are not yet myelinated. Up to the age of 20, large areas of the frontal lobes are not yet myelinated.1
Myelination begins in the developmentally oldest parts of the brain, like the brain stem, moving to the areas of the nervous system that have developed more recently, like the prefrontal lobe and cortex. Myelin spreads throughout the nervous system in stages, which vary slightly in each individual. Impairment of myelination can alter neural communication without necessarily causing severe CNS (central nervous system) damage.
The prefrontal portions of the cerebrum have a profound influence on human behavior.2 If an individual is injected with vaccines,most of which have adjuvants like mercury and aluminum compounds, as well as foreign proteins (some from other species in which the vaccines were grown) and biological organisms, unprotected nerves may be impacted. The argument for a role of vaccines in the development of autistic disorders hinges on these biological effects upon nerves, damaging them in a way that influences behavior and learning patterns.
The argument for adjuvants evoking an auto-immune response does not hinge on any inherent neuro-toxicity of these compounds, but on the initiation of an allergic response.
The model by which adjuvants initiate an immune response is that of Experimental Allergic Encephalomyelitis (EAE). To date, EAE is recognized as the best available animal model of several degenerative human diseases, like multiple sclerosis and post-vaccinal encephalopathies. EAE3 is generally thought to be an autoimmune response to myelin basic protein (MBP). Oddly, MBP can also suppress EAE, and many observations suggest that an independent immune response to so-called "adjuvant" material is also necessary to EAE induction. Of course, this is why adjuvants are used in vaccines, to dramatically increase the likelihood of an immune response to the administered biological material.
Thus, EAE may be a result of a pair of interactive immune responses, one against MBP, and one against the adjuvant. If so, the adjuvant should, like MBP, suppress EAE. Root-Bernstein, et al. (1986) presented data from experiments on strain 13 guinea pigs demonstrating EAE suppression by muramyl dipeptide, an active component of complete Freund's adjuvant. In the past, adjuvants have only been classified as immunopotentiators, not immunosuppressants. Apparently, adjuvants are both. This study strengthens the argument that adjuvants may be crucial to initiating an auto-immune response leading to post-vaccine neurological symptoms.
[Return to "Quick-Index" of Vaccines]

References

Edwards KM, Meade BD, Decker MD, et al. Comparison of 13 acellular pertussis vaccines: overview and serologic responses. Pediatrics 1995;96:548-57.
Orenstein WA, Brugliera PD. Preface: Immunization in medical education. Am J Prev Med 1994; 10(suppl):v-viii.
Root-Bernstein RS; Yurochko F; Westall FC. Clinical suppression of experimental allergic encephalomyelitis by muramyl dipeptide "adjuvant". Brain Res Bull, 17: 4, 1986 Oct, 473-6.
Written and overseen by Lewis Mehl-Madrona, M.D., Ph.D.
Program Director, Continuum Center for Health and Healing,Beth Israel Hospital / Albert Einstein School of Medicine
Website designed, hosted and maintained by The Healing Center On-Line © 2001

Myelin Sheath -Vaccines- Autism- Autoimmunity Discussed

What is in vaccines that might not be great for babies etc.

Auto-Immunity, Vaccines and Autism
V.K. Singh has studied autism as an autoimmune disorder for over fifteen years. He believes 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. He hypothesizes that an auto-immune reaction to basic brain structures, especially the myelin sheath, plays a critical role in causing the neurological impairments of patients with autism. He has suggested that an immune insult to developing myelin (after a natural infection or vaccination) causes "nicks" or small changes in the myelin sheath. These changes ultimately lead to life-long disturbances of higher mental functions such as learning, memory, communication, social interaction, etc.1
A disease is sometimes referred to as "autoimmune" when the etiology and pathogenesis is not well known or established. Autoimmunity is an abnormal immune reaction in which the immune system becomes primed to react against body organs, and the end result is autoimmune disease. Several factors contribute to the pathogenic mechanism of autoimmune diseases. These illnesses are commonly believed to be triggered by infectious agents; further, they are generally linked to genes that control immune responses. They cause immune abnormalities of T lymphocytes (one type of white blood cell); they induce the production of autoantibodies; they involve hormonal factors; and they generally show a gender preference.
This is also the case with autism: several autoimmune factors have been identified in patients with autism, suggesting the pathogenetic role of autoimmunity in autism. Some generalities regarding the genetics and immunology of autism are below:
Autism displays increased frequency of genetic factors for immune responses, e.g., HLA, C4B null allele and extended haplotypes. Autism involves a gender factor, i.e., it affects males about four times more than females. Autism often occurs in conjunction with a family history of autoimmune diseases, e.g., multiple sclerosis, rheumatoid arthritis, etc. Autism also involves hormonal factors, e.g., secretin, beta-endorphin, etc. Autism shows an association with infectious agents, in particular, viruses. Autistic patients have immune abnormalities, especially those that characterize an autoimmune reaction in a disease. Autistic patients also respond well to immune therapies.
The linkage of vaccines to neurological disorders comes through the promotion of an auto-immune process, triggered by the virus present in the vaccine together with the adjuvant used to sensitize the body to this virus. Wild viruses have also been linked to autism. Certain viral infections can easily be acquired during fetal life, infancy or early childhood. They can enter the brain through the nasopharyngeal membranes or induce an autoimmune response against the brain, thereby altering the development of brain function.
Since autism is an early-onset disorder, usually diagnosed before the age of 30 months, it has been suggested that viruses might serve as teratogens (agents that cause developmental malfunctions) contributing to autism.
Earlier studies implicated congenital rubella virus (RV), simply because children with this infection also showed autistic behaviors. Moreover, several autistic children did not produce antibodies to rubella vaccine even after the repeated rubella immunization. Although the reason for this problem has not been investigated, Singh believes it due to a defect in T lymphocytes reducing their functionality. In support of this, RV-induced lymphocyte proliferation response in autistic children was only one-fourth of the response in normal children.
A few cases of autism have also been described among children with congenital cytomegalovirus (CMV). Interestingly, an autistic child with CMV responded favorably to treatment with transfer factor, but there was no follow-up to the study in which this was reported. Singh and co-workers conducted a study of IgG antibodies to CMV. They found no statistical difference between autistic children and normal children.2 Simply put, this means that CMV is probably not related to autism.
Singh conducted a study of measles virus (MV) and human herpes virus-6 (HHV-6) in autism. This was done by two types of laboratory analysis: (a) virus antibody levels of MV and HHV-6; and (b) brain autoantibody titers in the same samples as those assayed for virus antibodies. This study showed that the virus antibody levels in the blood of autistic children were much higher when compared to normal children; and that the elevated virus antibody levels were associated with brain autoantibody titer. Interestingly, the viral antibody and brain autoantibody association was particularly true of MV antibody and MBP autoantibody (i.e., 90 percent of autistic children showed this association).
This observation led Singh to hypothesize that a measles virus-induced autoimmune response was a causal factor in autism, whereas HHV-6 via co-infection could also contribute to pathophysiology of the disorder. Although as yet unproven, Singh thinks it is an excellent working hypothesis to explain autism, and may also explain why some children show autistic regression after the measles-mumps-rubella (MMR) immunization. A small but significant proportion of children develop autism as a result of pre-or post-natal infections - for example, with rubella, cytomegalovirus, herpes simplex, HIV, and so on.3
William Shaw reports that he found none of the signs characteristic of known, inborn (genetic) metabolic disorders among children with autism and PDD (pages 31; 35-37; 68-9; 129). On pages 103-4 Shaw noted, "In several cases, electron microscopy has revealed live measles virus in the intestinal lining of children with the gastrointestinal abnormalities common in children with autism."
Since the brain is the affected organ in autism and other vaccine-induced neurological disorders, the autoimmune response will be directed against this organ. This response is commonly identified by certain autoimmune factors that have been identified in autistic children. The list includes brain-specific autoantibodies, viral antibodies, cytokine profile, immune activation markers, and antinuclear antibodies. Collectively, these are essential for identifying a brain-specific autoimmune response.
Brain autoantibody studies detect antibodies to two brain proteins - the myelin basic protein (MBP) and neuron-axon filament proteins (NAFP). The incidence of MBP antibody in the autistic population (70% positive) is over twenty times higher than that of the normal population (3% positive); hence, it serves as a primary marker of the autoimmune reaction in autism. In contrast, the incidence of NAFP antibody in autistic patients (55% positive) is only about twice that of normal controls (27% positive), making it a secondary marker of autoimmunity in autism.
Two immune activation markers or cytokines, namely interleukin-12 (IL-12) and interferon gamma (IFN-g), play key roles in the induction of autoimmune diseases, i.e., they initiate an autoimmune reaction. They are selectively elevated in autistic patients and should be measured as a sign of altered cellular autoimmunity - a function of Th-1 type white blood cells.
Virus serology measures levels of antibodies to measles (rubeola) virus (MV) and human herpes virus-6 (HHV-6). The antibody levels are elevated, which is a sign of a present infection, past infection, or reaction to 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.
Antinuclear antibodies (ANA) are non-specific antibodies often present in patients with autoimmune diseases. Approximately one-third of autistic children tested have positive titers of ANA. [Reference: V. Singh, 1992; unpublished data].
The induction of an auto-immune process against the central nervous system (particularly the myelin basic protein) may be the way that vaccines - coupled with their adjuvants - cause neurological damage, including seizures, autism, and encephalitis.4 Recently thirty-three autistic children (less than or equal to 10 years of age) were compared to controls which included 18 normal children (of the same ages), 20 children with idiopathic mental retardation (MR) of the same ages, 12 children with Down's syndrome (DS) of the same age, and 38 normal adults in the age range of 20 to 40 years.5
Antibodies to myelin basic protein were found in 19 of 33 (58%) sera from autistic children. In contrast, only 8 of 88 (9%) control sera were positive. Among these control sera, 3 of 20 (15%) sera were from MR children, 4 of 18 (22%) sera were from normal children, only one of 38 sera was from normal adults (25 to 40 years of age), but none of the 12 sera from the DS children showed this antibody positive reaction.
The authors suggested that the humoral, immune response to myelin basic protein (MBP) could be related in some way to mental retardation, since approximately 60% of autistic children had an IQ of 70 of lower. Seizure activity or antipsychotic drugs were not thought to relate to the production of anti-MBP, since there was neither the history of seizures nor the intake of antipsychotics (at least not at the time of blood drawing) among autistic or retarded children that were studied.
Immunological studies of autistic patients have revealed certain features that are also found in patients with other autoimmune diseases. There is a genetic predisposition for several autoimmune diseases6 , like grave's thyroid disease, rheumatoid arthritis, and insulin-dependant diabetes. Likewise, autism shows a greater concordance rate in monozygotic twins than in the normal population.7 Autism is also four to five times more prevalent in boys than in girls Ç a gender factor which is also seen in systemic lupus erythematosus (SLE), Grave's disease, and ankylosing spondylintis (though this is more common with women than men).
Triggering by microorganisms is thought to be an important feature of autoimmune diseases. Whether a similar event is associated with autism is not known but there are coincidental findings of congenital rubella8 and cytomegalovirus,9,10 indicating prior exposure to these microbial agents. Certain soluble antigens of immunocyte activation are elevated in the sera of autistic children,11 which is in concordance with similar findings in other autoimmune diseases, like SLE12 and multiple sclerosis.13
Forty to fifty percent of autistic patients show signs of depressed immunity, including reduced lymphocyte proliferation by phytohemagglutinin, concanavalin A, and pokeweed mitogens14,15,16 along with depression of the proportion of CD4+ T helper cells to suppresor-inducer (CD4CD45RA+) cells.17,18,19 They also showed reduced numbers of CD2+ T cells, CD4+ cells, and CD4+CD45RA+ lymphocytes,20 along with reduced B cells (CD20+) and a lower percentage of total lymphocytes than siblings and normal children.21
The level of blood values for female subjects appeared lower than those for males as compared to normal subjects of the same sex. While family and twin studies support a genetic component for autistic spectrum disorders, children with autism, also have increased eosinophil and basophil response to IgE-mediated reactions.22
A cause and effect relationship between antibodies to myelin basic protein (MBP) and autism has not yet been definitively established. There may be many routes to autism, of which auto-immunity is only one. Nevertheless, the development of antibodies to MBP may be a major route through which vaccination contributes to autism.
Another possibility for post-vaccine related damage is delayed or incomplete myelination in the corpus callosum (the largest myelinated area of the brain), which has been suggested as a basis for auditory processing problems in some children with learning disabilities (LD).23 Immunological assaults from wild virus infection or vaccine virus infection could theoretically result in poor myelination or abnormal function of the neuron-axon myelin.
[Return to "Quick-Index" of Vaccines]

References

Singh VK. Autism, Autoimmunity and Immunotherapy: a Commentary, Autism Autoimmunity Project.
V. Singh, D. Schubert and R. Warren, 1992; unpublished data.
Cohen and Volkmar, eds., Handbook of Autism and Pervasive Developmental Disorders, 2nd edition, 1997: p. 398.
Singh VK. CD4+ Helper T Cell Depression in Autism. Immunology Letters, 1990; 25(4): 341-5.
Brain, Behavior, and Immunity 7, 97-103 (1993).
Shoenfeld, Y., & Isenberg, D. (1989). The genetic components in autoimmunity. In The Mosaic of Autoimmunity, chap. 5, pp. 169-228. Elsevier: Amsterdam.
Folstein, S., & Rutter M. (1988). Autism: Familial aggregation and genetic implications. J. Aut. Develop. Disord. 18, 3-30.
Chess, S. (1971). Autism in children with congenital rubella. J. Aut. Childh. Schizophr. 1, 33-47.
Ivarsson, S. A., Bjerre, I., Vegfors, P., & Ahlfors, K. (1990). Autism as one of several abnormalities in two children with congenital cytomegalovirus infection. Neuropediatrics 21, 102-103.
Stubbs, E.G. (1987). Does intrauterine cytomegalovirs plus autoantibodies contribute to autism? In L. Wing (Ed.), Aspects of Autism: Biological Research, Gaskell Psychiatry Series, pp. 91-101.
Singh, V. K., Warren, R.P., Odell, J.D., & Cole, P. (1991). Changes of soluble interleukin-2, interleukin-2 receptor, T8 antigen, and interleukin-1 in the serum of autistic children. Clin. Immunol. Immunopath. 61, 448-455.
Huang, Y.P., Perrin, L.H., Miescher, P.A., & Zubler, R.H. (1988). Coorelation of T and B cell activites in vitro and serum IL-2 levels in systemic lupus erythematosus. J. Immunol. 141, 827-833.
Trotter, J.L., Clifford, D. B., Anderson, C. B., van der Veen, R. C., Hicks, B.C., & Banks, G. (1988). Elevated serum interleukin-2 levels in chronic progressive multiple sclerosis. N. Engl. J. Med. 318, 1206.
Singh, V. K., Fudenberg, H.H., Emerson, D., & Coleman, M. (1988). Immunodiagnosis and immunotherapy in autistic children. Ann. N.Y. Acad. Sci. 540, 602-604.
Stubbs, E.G. Crawford, M. L., Burger, D.R., & Vandenbark, A. A. (1977). Depressed lymphocyte responsiveness in autistic children. J. Aut. Childh. Schizophr. 7, 49-55.
Warren, R. P., Foster, A., Margretten, N. C., & Pace, N. C. (1986). Immune abnormalities in patients with autism. J. Aut. Dev. Disord. 16, 189-197.
Warren, R. P., Yonk, L. J., Burger, R.A., Cole, P., Odell, J. D., Warren, W. L., White, E., & Singh, V. K. (1990). Deficiency of suppressor-inducer (CD4 + Cd45RA + ) T cells in autism. Immunol. Invest. 19, 245-251.
Yonk, L. J., Warren, R. P., Burger, R. A., Cole, P., Odell, J. D., Warren, W. L., White, E., & Singh, V. K. (1990). CD4+ helper T cell depression in autism. Immunol. Lett. 25, 341-346.
Singh VK. Changes of Soluble Interleukin-2, Interleukin-2 Receptor, T8 Antigen, and Interleukin-1 in the Serum of Autistic Children. Clinical Immunology and Immunopathology, 1991; 61(3): 448-455.
Singh VK. Deficiency of Suppressor-inducer (CD4+CD45RA+) T Cells in Autism. Immunological Investigations, 1990; 19(3): 245-51.
Singh VK. CD4+ Helper T Cell Depression in Autism. Immunology Letters, 1990; 25(4): 341-5.
Trottier G. Etiology of infantile autism: a review of recent advances in genetic and neurobiological research. Journal of Psychiatry and Neuroscience, 1999; 24(2): 103-15.
Musiek, F. E., Gollegly, K. M., & Baran, J. A. (1984). Myelination of the corpus callosum and auditory processing problems in children: theoretical and clinical correlates. Semin. Hearing 5, 231-241.
Written and overseen by Lewis Mehl-Madrona, M.D., Ph.D.
Program Director, Continuum Center for Health and Healing,Beth Israel Hospital / Albert Einstein School of Medicine
Website designed, hosted and maintained by The Healing Center On-Line © 2001