Re: Autism tests and treatments - recommened by Dr Singh

[Guest guest]

Hi Natasa,

I was just looking.

http://www.zoominfo.com/Search/PersonDetail.aspx?PersonID=3769598

He looks like a doctor that spoke at the DAN! recovered children -

I'm wondering if he was the doctor who recovered the first boy (was

it the mum that saw him as the 40th doctor - the boy who went on to

study film? my memory may be going though)

A quick aside ... Do you keep coming to whale.to?

http://www.whale.to/vaccines/singh.html was the 2nd Google link on

this doctors name. I find this site has come up a lot here and

there. Also educate-yourself http://educate-yourself.org/. It's all

an alternative educcation for me ... and very interesting too if only

I had more time to read :-)!

But this Dr Singh looks amazing - I don't imagine he consults by

phone ... ?

Best wishes,

Sandy

>

> ... I find it very odd that his findings and suggestions have not

been

> explored by DAN! and others to greater extent!

>

> I have saved the text below a while ago, someone brought up

discussion

> on one of the treatments..

>

> here is a bit more on his work:

> http://www.latitudes.org/articles/singh_neuro_ts.html

>

>

> 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

>

> Autism is an early-onset biological disorder that causes severe

> deficits of higher mental functions, as well as behavioral

> manifestations. There is no single, clear-cut cause and no complete

> cure for autism. Causally speaking, immune factors, neuro-chemical

> factors, genetic susceptibility factors and environmental factors

(such

> as microbial infections and chemical toxicity) have been

implicated. I

> view autism as a very complex, multifactorial disorder. In this

> article, I will attempt to describe succinctly the role of

autoimmune

> etiology and immune therapy for autism.

>

> As a neuroimmunologist, I have been interested in the immunology of

the

> nervous system, i.e., the immune basis and immune therapy for brain

> diseases and mental illnesses. I have studied autism as an

autoimmune

> disorder for over fifteen years. As a result, 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. I recently postulated a

> " Neuroautoimmunity Model of Autism " which I discussed at two recent

> conferences: first, the Biomedical Treatments for Autism and PDD

> Conference held in Orlando, Florida (May, 1999); and second, the

> Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

Bethesda,

> land (June, 1999). Briefly, I hypothesized that an autoimmune

> reaction to brain structures, in particular the myelin sheath,

plays a

> critical role in causing the neurological impairments of patients

with

> autism. I 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.

>

> I believe that autism can be treated successfully using some of the

> therapies proven effective in treating other autoimmune diseases. I

am

> exploring specifically the role of autoimmune factors, (e.g.,

viruses,

> autoantibodies, T cells, and cytokines) because they serve as the

prime

> targets of therapy with immune-modulating agents. I emphasize the

need

> to focus on immunotherapies, and I urge doctors toexamine

autoimmunity

> as a novel target on which to focus in treating autistic patients.

> There is enormous potential for restoring brain function in

autistic

> children and adults through immunology.

>

> Autoimmune Etiology in Autism

>

> A disease is commonly 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. While

some

> of the key features are listed below, I will focus more on the

current

> research relating to three topics: viral studies; autoimmune

testing;

> and autoimmune therapy. 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, extended haplotypes, etc.

>

> 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 respond well to immune therapies.

>

> Viral Studies in Autism

>

> Viruses have been linked to autism, but this relationship is far

from

> fully explored. 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 was 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 never been investigated, I think

this

> is due to a defect in T lymphocytes-these agents of immune response

are

> not functioning properly in these children. In an unpublished pilot

> study, I found that the RV-induced lymphocyte proliferation

response in

> autistic children was only one-fourth of the response in normal

> children, which clearly suggests a defect of T cell-mediated

immunity

> (a defense mechanism that helps fight virus infections).

>

> 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. A few

years

> ago I and coworkers conducted a study of IgG antibodies to CMV; we

> found no statistical difference between autistic children and

normal

> children (V. Singh, D. Schubert and R. Warren, 1992; unpublished

data).

> Simply put, this means that CMV is probably not related to autism.

>

> More recently, I conducted a study of measles virus (MV) and human

> herpesvirus-6 (HHV-6) in autism. This was done by two types of

> laboratory analysis: (a) virus antibody levels of MV and HHV-6; and

(

> brain autoantibody titers in the same samples as those assayed for

> virus antibodies. 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

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 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.

>

> Testing for Autoimmunity in Autism

>

> Recent advances have clearly shown that autoimmunity plays a key

role

> in the pathogenesis of autism. Since the brain is the affected

organ in

> autism, the autoimmune response will be directed against this

organ.

> This response is commonly identified by certain autoimmune factors

> which I have identified in autistic children. The list includes

> brain-specific autoantibodies, viral antibodies, cytokine profile

or

> immune activation markers, as well as antinuclear antibodies.

> Collectively, they are essential for identifying a brain-specific

> autoimmune response, which can afterward be treated with immune

> therapy. By performing blood tests we can determine if a patient

shows

> autoimmunity to brain tissues, if he or she is a candidate for

> experimental immune therapy, and if the response to therapy is

> effective. Therefore, this type of immune evaluation is very

important

> in helping children with autism.

>

> Brain autoantibodies: this test detects antibodies to two brain

> proteins, namely 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. It is, however, recommended that the two

> markers be tested simultaneously.

>

> Cytokine profile: 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: this test 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: this test assays for antinuclear antibodies

> (ANA). They are non-specific antibodies but are often present in

> patients with autoimmune diseases. Approximately one-third of

autistic

> children tested have positive titers of ANA (V. Singh, 1992;

> unpublished data).

>

> Immunotherapy in Autism

>

> The aforementioned laboratory findings clearly point to an

autoimmune

> pathogenic mechanism in autism. The idea that autism is an

autoimmune

> disorder is further strengthened by the fact that autistic patients

> respond well to treatment with immune modulating drugs. Immune

> interventions can produce immune modulation-a state of suppression

or

> stimulation. Depending on the nature of the immune abnormality, 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. Immune therapy should always be done in

consultation

> with physicians. The following immune interventions can be used:

>

> Steroid therapy: steroids such as Prednisone and/or ACTH

> (adrenocorticotropin hormone) are commonly used as anti-

inflammatory

> and/or immunosuppressive drugs for treating patients with

autoimmune

> diseases, inflammatory diseases, etc. In autism, however, there is

only

> one study that showed improvement of autistic-like symptoms in

children

> when they were treated with an ACTH analogue. This result indicated

> that steroids are potentially useful in alleviating clinical

symptoms

> of autism. Steroids are the first course of treatment for patients

with

> autoimmune diseases and infantile spasm; however, their efficacy

has

> not been evaluated in autism.

>

> Intraveneous immunoglobulin (IVIG): this type of treatment has been

> used to treat children with autism. Open-label trials of both low-

dose

> and high-dose IVIG have shown that most but not all autistic

children

> respond favorably to this treatment. My collaborators and I

recently

> found that the high-dose IVIG was better than the low-dose IVIG (J.

> Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> International Symposium on Autism, Netherlands, December 28-30,

1999).

> Clinically, children so treated have shown improvements in

language,

> communication, social interaction and attention span. In a double-

blind

> study, (V. Singh, 1997; unpublished data) the IVIG treatment was

found

> to decrease brain autoantibody titers in five patients (they were

> positive pre-therapy but became virtually negative post-therapy)

who

> also showed clinical improvement of autistic characteristics. In

spite

> of the success of IVIG, this treatment is not for everyone. Before

this

> treatment is administered, a proper immune evaluation is highly

> recommended to assess the nature of the immune problem.

>

> Oral tolerance with autoantigens: this treatment is a means of

inducing

> immune suppression by feeding patients autoantigen. I have shown

that

> the candidate autoantigen in autism appeared to be a myelin basic

> protein (MBP); this suggested that the MBP-containing myelin

products

> can be used to treat autistic patients. Indeed, one such product

known

> as Sphingolin has been used with success. Recently, the parents,

school

> psychologists, and other professionals have anecdotally reported

> tremendous improvements of autistic symptoms in their children.

These

> reports are undoubtedly quite encouraging and promising, but a

> well-designed clinical trial is warranted.

>

> Plasmapheresis: although it is not commonly recommended, this

procedure

> is used for treating patients with infections, autoimmune diseases,

> immune complex diseases, etc. Because this method removes harmful

> substances (e.g., autoantibodies) from the blood, it is considered

a

> viable immune therapy. The method has been used to treat certain

brain

> disorders, for example Rasmussen's encephalitis (RE) and

> obsessive-compulsive disorder (OCD), in which autoimmunity has been

> implicated as a basis of the disorder. Plasmapheresis produced

positive

> responses in patients with these disorders, and the responses were

much

> better with plasmapheresis when compared to the IVIG treatment. In

each

> case, the benefit to the patient was associated with the lowering

of

> the anti-neuronal antibody titers. Since autistic patients also

have

> positive titers of brain autoantibodies, they should also respond

to

> plasmapheresis. Although this treatment has long been suggested

for use

> in autism (V. Singh, 1997), plasmapheresis has thus far not been

tried

> in patients with this disorder.

>

> Conclusion

>

> The evidence is rapidly accumulating to suggest that autism is an

> autoimmune disorder. The autoimmune response is most likely

directed

> against the brain myelin, perhaps secondary to a viral infection.

> Measles virus is a candidate but other possibilities remain to be

> explored. More importantly, the patients respond to treatment with

> immune therapies. Therefore, I conclude that autoimmunity

offersstrong

> prospects for drug discovery and therapy for autism. Naturally, it

> deserves prompt attention from all those who want to help people

with

> autism.

>

> Selected Reading

>

> Singh, V. K., " Plasma Increase of Interleukin-12 and Interferon-

gamma:

> Pathological Significance in Autism " (Journal of Neuroimmunology,

vol.

> 66, pp. 143-145 [1996]).

>

> Singh, V. K., " Immunotherapy for Brain Diseases and Mental

Illnesses, "

> (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

>

> Singh, V. K., " Serological Association of Measles Virus and Human

> Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

Immunology

> and Immunopathology, vol. 89, pp. 105-108 [1998]).

>

> Singh, V. K., " Autoimmunity and Neurologic Disorders " (Latitudes,

vol.

> 4, pp. 5-11 [1999]).

>

> Dr. Singh received his doctorate from the University of British

> Columbia, Vancouver, Canada. His post-doctoral fellowship was

completed

> in neurochemistry and neuroimmunology. Spanning over twenty years'

> experience in neurobiology and immunology research, Dr. Singh

studied

> brain diseases, particularly infantile autism and Alzheimer's

disease.

> Having authored over a hundred scientific publications, he is both

a

> pioneer and an international authority on autoimmunity in autism.

Dr.

> Singh is a member of the American Association for the Advancement

of

> Sciences, the American Association of Immunologists, and the New

York

> Academy of Sciences. He is listed in American Men and Women in

Science

> (United States, R. R. Bowker, publisher) and The International

Who's

> Who of Intellectuals (Cambridge, England, International

Biographical

> Centre).

>

> For further information, please contact Dr. Vijendra Singh, Ph.D.,

at

> the Biotechnology Center, Department of Biology, Utah State

University,

> 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> singhvk@...].

>

> Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,

vol. 1,

> number 2, December 1999.

>

>

>

> Links

>

> " Autoimmunity and Neurological Disorders, " interview with V. K.

Singh in

> Latitudes, newsletter of the Association for

> Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,

vol. 4,

> no. 2, Spring 1999, by Sheila

> : http://lib.tcu.edu/www/staff/lruede/latitudes

>

> " V. K. Singh: Selected Research on Autism, "

http://www.gti.net/truegrit/

> : Findings in Immunology

>

> " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease, "

> (http://lib.tcu.edu/www/staff/lruede/alzheimers)

>

>

>

>

> > __________________________________________________

> > Correo Yahoo!

> > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > Regístrate ya - http://correo.espanol.yahoo.com/

> >

>

[Guest guest]

me again, just re-read stuff on the link below, have a look at this bit:"...The other treatment, which readers must understand is based on anecdotal reports, is Sphingolin treatment. Sphingolin is a trade name for a bovine brain myelin preparation. This commercial product is sold as a nutritional supplement and can be used to correct the immune response against the myelin basic protein. So, if the child is found to have antibodies to myelin basic protein or even neurofilaments, which are rich in myelin components, then you may think about giving this treatment. Many of those who have done so are noticing very positive responses. I have parents who insist they would not consider taking their autistic child off this treatment; I have a folder full of parent correspondence on this, but studies are yet to be done. The important thing is to first check whether the child has antibodies to myelin basic protein or neurofilament. If there are no antibodies, don't do this treatment.We do not yet know how Sphingolin works, but the mechanism of oral tolerance induction might be involved. While the exact mechanism of oral tolerance is not known, it is an exciting topic of research for hard-core immunologists today. LetÕs say that we have a situation where the autoimmune response to myelin is being defined reasonably well in autistic children. When you feed autoantigensÑin this case the SphingolinÑto these children, it can result in remarkable recovery. This is anecdotal but recorded not only by school psychologists, teachers, and parents, but also by physicians who are involved. This is very exciting. Dosage should not be high; it should be quite low to have this benefit to the patient. I'm not a physician and don't prescribe treatment, so I am not advising your readers on a specific approach. But from a research standpoint, in my opinion, the adult dose is generally two capsules per day, hence the child would take only one or one-half. We are trying to raise funds for a clinical trial of this...."wonder if this test is something that a DAN! could order? has anyone here had it done? (Immunosciences Lab?)natasa>> ... I find it very odd that his findings and suggestions have not been> explored by DAN! and others to greater extent!> > I have saved the text below a while ago, someone brought up discussion> on one of the treatments..> > here is a bit more on his work:> http://www.latitudes.org/articles/singh_neuro_ts.html> > > 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> > Autism is an early-onset biological disorder that causes severe > deficits of higher mental functions, as well as behavioral > manifestations. There is no single, clear-cut cause and no complete > cure for autism. Causally speaking, immune factors, neuro-chemical > factors, genetic susceptibility factors and environmental factors (such > as microbial infections and chemical toxicity) have been implicated. I > view autism as a very complex, multifactorial disorder. In this > article, I will attempt to describe succinctly the role of autoimmune > etiology and immune therapy for autism.> > As a neuroimmunologist, I have been interested in the immunology of the > nervous system, i.e., the immune basis and immune therapy for brain > diseases and mental illnesses. I have studied autism as an autoimmune > disorder for over fifteen years. As a result, 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. I recently postulated a > "Neuroautoimmunity Model of Autism" which I discussed at two recent > conferences: first, the Biomedical Treatments for Autism and PDD > Conference held in Orlando, Florida (May, 1999); and second, the > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in Bethesda, > land (June, 1999). Briefly, I hypothesized that an autoimmune > reaction to brain structures, in particular the myelin sheath, plays a > critical role in causing the neurological impairments of patients with > autism. I 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.> > I believe that autism can be treated successfully using some of the > therapies proven effective in treating other autoimmune diseases. I am > exploring specifically the role of autoimmune factors, (e.g., viruses, > autoantibodies, T cells, and cytokines) because they serve as the prime > targets of therapy with immune-modulating agents. I emphasize the need > to focus on immunotherapies, and I urge doctors toexamine autoimmunity > as a novel target on which to focus in treating autistic patients. > There is enormous potential for restoring brain function in autistic > children and adults through immunology.> > Autoimmune Etiology in Autism> > A disease is commonly 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. While some > of the key features are listed below, I will focus more on the current > research relating to three topics: viral studies; autoimmune testing; > and autoimmune therapy. 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, extended haplotypes, etc.> > 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 respond well to immune therapies.> > Viral Studies in Autism> > Viruses have been linked to autism, but this relationship is far from > fully explored. 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 was 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 never been investigated, I think this > is due to a defect in T lymphocytes-these agents of immune response are > not functioning properly in these children. In an unpublished pilot > study, I found that the RV-induced lymphocyte proliferation response in > autistic children was only one-fourth of the response in normal > children, which clearly suggests a defect of T cell-mediated immunity > (a defense mechanism that helps fight virus infections).> > 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. A few years > ago I and coworkers conducted a study of IgG antibodies to CMV; we > found no statistical difference between autistic children and normal > children (V. Singh, D. Schubert and R. Warren, 1992; unpublished data). > Simply put, this means that CMV is probably not related to autism.> > More recently, I conducted a study of measles virus (MV) and human > herpesvirus-6 (HHV-6) in autism. This was done by two types of > laboratory analysis: (a) virus antibody levels of MV and HHV-6; and ( > brain autoantibody titers in the same samples as those assayed for > virus antibodies. 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 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 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.> > Testing for Autoimmunity in Autism> > Recent advances have clearly shown that autoimmunity plays a key role > in the pathogenesis of autism. Since the brain is the affected organ in > autism, the autoimmune response will be directed against this organ. > This response is commonly identified by certain autoimmune factors > which I have identified in autistic children. The list includes> brain-specific autoantibodies, viral antibodies, cytokine profile or> immune activation markers, as well as antinuclear antibodies. > Collectively, they are essential for identifying a brain-specific > autoimmune response, which can afterward be treated with immune > therapy. By performing blood tests we can determine if a patient shows > autoimmunity to brain tissues, if he or she is a candidate for> experimental immune therapy, and if the response to therapy is> effective. Therefore, this type of immune evaluation is very important> in helping children with autism.> > Brain autoantibodies: this test detects antibodies to two brain > proteins, namely 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. It is, however, recommended that the two > markers be tested simultaneously.> > Cytokine profile: 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: this test 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: this test assays for antinuclear antibodies> (ANA). They are non-specific antibodies but are often present in> patients with autoimmune diseases. Approximately one-third of autistic> children tested have positive titers of ANA (V. Singh, 1992;> unpublished data).> > Immunotherapy in Autism> > The aforementioned laboratory findings clearly point to an autoimmune > pathogenic mechanism in autism. The idea that autism is an autoimmune > disorder is further strengthened by the fact that autistic patients > respond well to treatment with immune modulating drugs. Immune > interventions can produce immune modulation-a state of suppression or > stimulation. Depending on the nature of the immune abnormality, 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. Immune therapy should always be done in consultation > with physicians. The following immune interventions can be used:> > Steroid therapy: steroids such as Prednisone and/or ACTH> (adrenocorticotropin hormone) are commonly used as anti-inflammatory> and/or immunosuppressive drugs for treating patients with autoimmune> diseases, inflammatory diseases, etc. In autism, however, there is only> one study that showed improvement of autistic-like symptoms in children> when they were treated with an ACTH analogue. This result indicated> that steroids are potentially useful in alleviating clinical symptoms> of autism. Steroids are the first course of treatment for patients with> autoimmune diseases and infantile spasm; however, their efficacy has> not been evaluated in autism.> > Intraveneous immunoglobulin (IVIG): this type of treatment has been> used to treat children with autism. Open-label trials of both low-dose> and high-dose IVIG have shown that most but not all autistic children> respond favorably to this treatment. My collaborators and I recently> found that the high-dose IVIG was better than the low-dose IVIG (J.> Bradstreet, V. Singh and J. El-Dahr, paper presented at the> International Symposium on Autism, Netherlands, December 28-30, 1999).> Clinically, children so treated have shown improvements in language,> communication, social interaction and attention span. In a double-blind> study, (V. Singh, 1997; unpublished data) the IVIG treatment was found> to decrease brain autoantibody titers in five patients (they were> positive pre-therapy but became virtually negative post-therapy) who> also showed clinical improvement of autistic characteristics. In spite> of the success of IVIG, this treatment is not for everyone. Before this> treatment is administered, a proper immune evaluation is highly> recommended to assess the nature of the immune problem.> > Oral tolerance with autoantigens: this treatment is a means of inducing > immune suppression by feeding patients autoantigen. I have shown that > the candidate autoantigen in autism appeared to be a myelin basic > protein (MBP); this suggested that the MBP-containing myelin products > can be used to treat autistic patients. Indeed, one such product known > as Sphingolin has been used with success. Recently, the parents, school> psychologists, and other professionals have anecdotally reported > tremendous improvements of autistic symptoms in their children. These > reports are undoubtedly quite encouraging and promising, but a > well-designed clinical trial is warranted.> > Plasmapheresis: although it is not commonly recommended, this procedure> is used for treating patients with infections, autoimmune diseases,> immune complex diseases, etc. Because this method removes harmful> substances (e.g., autoantibodies) from the blood, it is considered a> viable immune therapy. The method has been used to treat certain brain> disorders, for example Rasmussen's encephalitis (RE) and> obsessive-compulsive disorder (OCD), in which autoimmunity has been> implicated as a basis of the disorder. Plasmapheresis produced positive> responses in patients with these disorders, and the responses were much> better with plasmapheresis when compared to the IVIG treatment. In each> case, the benefit to the patient was associated with the lowering of> the anti-neuronal antibody titers. Since autistic patients also have> positive titers of brain autoantibodies, they should also respond to> plasmapheresis. Although this treatment has long been suggested for use> in autism (V. Singh, 1997), plasmapheresis has thus far not been tried> in patients with this disorder.> > Conclusion> > The evidence is rapidly accumulating to suggest that autism is an > autoimmune disorder. The autoimmune response is most likely directed > against the brain myelin, perhaps secondary to a viral infection. > Measles virus is a candidate but other possibilities remain to be > explored. More importantly, the patients respond to treatment with > immune therapies. Therefore, I conclude that autoimmunity offersstrong > prospects for drug discovery and therapy for autism. Naturally, it > deserves prompt attention from all those who want to help people with > autism.> > Selected Reading> > Singh, V. K., "Plasma Increase of Interleukin-12 and Interferon-gamma: > Pathological Significance in Autism" (Journal of Neuroimmunology, vol. > 66, pp. 143-145 [1996]).> > Singh, V. K., "Immunotherapy for Brain Diseases and Mental Illnesses,"> (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).> > Singh, V. K., "Serological Association of Measles Virus and Human > Herpesvirus-6 With Brain Autoantibodies in Autism" (Clinical Immunology > and Immunopathology, vol. 89, pp. 105-108 [1998]).> > Singh, V. K., "Autoimmunity and Neurologic Disorders" (Latitudes, vol.> 4, pp. 5-11 [1999]).> > Dr. Singh received his doctorate from the University of British > Columbia, Vancouver, Canada. His post-doctoral fellowship was completed > in neurochemistry and neuroimmunology. Spanning over twenty years' > experience in neurobiology and immunology research, Dr. Singh studied > brain diseases, particularly infantile autism and Alzheimer's disease. > Having authored over a hundred scientific publications, he is both a > pioneer and an international authority on autoimmunity in autism. Dr. > Singh is a member of the American Association for the Advancement of > Sciences, the American Association of Immunologists, and the New York > Academy of Sciences. He is listed in American Men and Women in Science > (United States, R. R. Bowker, publisher) and The International Who's > Who of Intellectuals (Cambridge, England, International Biographical > Centre).> > For further information, please contact Dr. Vijendra Singh, Ph.D., at > the Biotechnology Center, Department of Biology, Utah State University, > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail: > singhvk@...].> > Reprinted from AAPN, The Autism Autoimmunity Project Newsletter, vol. 1,> number 2, December 1999.> > > > Links> > "Autoimmunity and Neurological Disorders," interview with V. K. Singh in> Latitudes, newsletter of the Association for> Comprehensive NeuroTherapy, http://www.latitudes.org/index.html, vol. 4,> no. 2, Spring 1999, by Sheila> : http://lib.tcu.edu/www/staff/lruede/latitudes> > "V. K. Singh: Selected Research on Autism," http://www.gti.net/truegrit/> : Findings in Immunology> > "Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease,"> (http://lib.tcu.edu/www/staff/lruede/alzheimers)> > > > > > __________________________________________________> > Correo Yahoo!> > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!> > Regístrate ya - http://correo.espanol.yahoo.com/> >>

[Guest guest]

> >

> > ... I find it very odd that his findings and suggestions have not

> been

> > explored by DAN! and others to greater extent!

> >

> > I have saved the text below a while ago, someone brought up

> discussion

> > on one of the treatments..

> >

> > here is a bit more on his work:

> > http://www.latitudes.org/articles/singh_neuro_ts.html

> >

> >

> > 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

> >

> > Autism is an early-onset biological disorder that causes severe

> > deficits of higher mental functions, as well as behavioral

> > manifestations. There is no single, clear-cut cause and no complete

> > cure for autism. Causally speaking, immune factors, neuro-chemical

> > factors, genetic susceptibility factors and environmental factors

> (such

> > as microbial infections and chemical toxicity) have been

> implicated. I

> > view autism as a very complex, multifactorial disorder. In this

> > article, I will attempt to describe succinctly the role of

> autoimmune

> > etiology and immune therapy for autism.

> >

> > As a neuroimmunologist, I have been interested in the immunology of

> the

> > nervous system, i.e., the immune basis and immune therapy for brain

> > diseases and mental illnesses. I have studied autism as an

> autoimmune

> > disorder for over fifteen years. As a result, 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. I recently postulated a

> > " Neuroautoimmunity Model of Autism " which I discussed at two recent

> > conferences: first, the Biomedical Treatments for Autism and PDD

> > Conference held in Orlando, Florida (May, 1999); and second, the

> > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

> Bethesda,

> > land (June, 1999). Briefly, I hypothesized that an autoimmune

> > reaction to brain structures, in particular the myelin sheath,

> plays a

> > critical role in causing the neurological impairments of patients

> with

> > autism. I 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.

> >

> > I believe that autism can be treated successfully using some of the

> > therapies proven effective in treating other autoimmune diseases. I

> am

> > exploring specifically the role of autoimmune factors, (e.g.,

> viruses,

> > autoantibodies, T cells, and cytokines) because they serve as the

> prime

> > targets of therapy with immune-modulating agents. I emphasize the

> need

> > to focus on immunotherapies, and I urge doctors toexamine

> autoimmunity

> > as a novel target on which to focus in treating autistic patients.

> > There is enormous potential for restoring brain function in

> autistic

> > children and adults through immunology.

> >

> > Autoimmune Etiology in Autism

> >

> > A disease is commonly 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. While

> some

> > of the key features are listed below, I will focus more on the

> current

> > research relating to three topics: viral studies; autoimmune

> testing;

> > and autoimmune therapy. 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, extended haplotypes, etc.

> >

> > 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 respond well to immune therapies.

> >

> > Viral Studies in Autism

> >

> > Viruses have been linked to autism, but this relationship is far

> from

> > fully explored. 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 was 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 never been investigated, I think

> this

> > is due to a defect in T lymphocytes-these agents of immune response

> are

> > not functioning properly in these children. In an unpublished pilot

> > study, I found that the RV-induced lymphocyte proliferation

> response in

> > autistic children was only one-fourth of the response in normal

> > children, which clearly suggests a defect of T cell-mediated

> immunity

> > (a defense mechanism that helps fight virus infections).

> >

> > 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. A few

> years

> > ago I and coworkers conducted a study of IgG antibodies to CMV; we

> > found no statistical difference between autistic children and

> normal

> > children (V. Singh, D. Schubert and R. Warren, 1992; unpublished

> data).

> > Simply put, this means that CMV is probably not related to autism.

> >

> > More recently, I conducted a study of measles virus (MV) and human

> > herpesvirus-6 (HHV-6) in autism. This was done by two types of

> > laboratory analysis: (a) virus antibody levels of MV and HHV-6; and

> (

> > brain autoantibody titers in the same samples as those assayed for

> > virus antibodies. 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

> 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 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.

> >

> > Testing for Autoimmunity in Autism

> >

> > Recent advances have clearly shown that autoimmunity plays a key

> role

> > in the pathogenesis of autism. Since the brain is the affected

> organ in

> > autism, the autoimmune response will be directed against this

> organ.

> > This response is commonly identified by certain autoimmune factors

> > which I have identified in autistic children. The list includes

> > brain-specific autoantibodies, viral antibodies, cytokine profile

> or

> > immune activation markers, as well as antinuclear antibodies.

> > Collectively, they are essential for identifying a brain-specific

> > autoimmune response, which can afterward be treated with immune

> > therapy. By performing blood tests we can determine if a patient

> shows

> > autoimmunity to brain tissues, if he or she is a candidate for

> > experimental immune therapy, and if the response to therapy is

> > effective. Therefore, this type of immune evaluation is very

> important

> > in helping children with autism.

> >

> > Brain autoantibodies: this test detects antibodies to two brain

> > proteins, namely 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. It is, however, recommended that the two

> > markers be tested simultaneously.

> >

> > Cytokine profile: 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: this test 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: this test assays for antinuclear antibodies

> > (ANA). They are non-specific antibodies but are often present in

> > patients with autoimmune diseases. Approximately one-third of

> autistic

> > children tested have positive titers of ANA (V. Singh, 1992;

> > unpublished data).

> >

> > Immunotherapy in Autism

> >

> > The aforementioned laboratory findings clearly point to an

> autoimmune

> > pathogenic mechanism in autism. The idea that autism is an

> autoimmune

> > disorder is further strengthened by the fact that autistic patients

> > respond well to treatment with immune modulating drugs. Immune

> > interventions can produce immune modulation-a state of suppression

> or

> > stimulation. Depending on the nature of the immune abnormality, 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. Immune therapy should always be done in

> consultation

> > with physicians. The following immune interventions can be used:

> >

> > Steroid therapy: steroids such as Prednisone and/or ACTH

> > (adrenocorticotropin hormone) are commonly used as anti-

> inflammatory

> > and/or immunosuppressive drugs for treating patients with

> autoimmune

> > diseases, inflammatory diseases, etc. In autism, however, there is

> only

> > one study that showed improvement of autistic-like symptoms in

> children

> > when they were treated with an ACTH analogue. This result indicated

> > that steroids are potentially useful in alleviating clinical

> symptoms

> > of autism. Steroids are the first course of treatment for patients

> with

> > autoimmune diseases and infantile spasm; however, their efficacy

> has

> > not been evaluated in autism.

> >

> > Intraveneous immunoglobulin (IVIG): this type of treatment has been

> > used to treat children with autism. Open-label trials of both low-

> dose

> > and high-dose IVIG have shown that most but not all autistic

> children

> > respond favorably to this treatment. My collaborators and I

> recently

> > found that the high-dose IVIG was better than the low-dose IVIG (J.

> > Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> > International Symposium on Autism, Netherlands, December 28-30,

> 1999).

> > Clinically, children so treated have shown improvements in

> language,

> > communication, social interaction and attention span. In a double-

> blind

> > study, (V. Singh, 1997; unpublished data) the IVIG treatment was

> found

> > to decrease brain autoantibody titers in five patients (they were

> > positive pre-therapy but became virtually negative post-therapy)

> who

> > also showed clinical improvement of autistic characteristics. In

> spite

> > of the success of IVIG, this treatment is not for everyone. Before

> this

> > treatment is administered, a proper immune evaluation is highly

> > recommended to assess the nature of the immune problem.

> >

> > Oral tolerance with autoantigens: this treatment is a means of

> inducing

> > immune suppression by feeding patients autoantigen. I have shown

> that

> > the candidate autoantigen in autism appeared to be a myelin basic

> > protein (MBP); this suggested that the MBP-containing myelin

> products

> > can be used to treat autistic patients. Indeed, one such product

> known

> > as Sphingolin has been used with success. Recently, the parents,

> school

> > psychologists, and other professionals have anecdotally reported

> > tremendous improvements of autistic symptoms in their children.

> These

> > reports are undoubtedly quite encouraging and promising, but a

> > well-designed clinical trial is warranted.

> >

> > Plasmapheresis: although it is not commonly recommended, this

> procedure

> > is used for treating patients with infections, autoimmune diseases,

> > immune complex diseases, etc. Because this method removes harmful

> > substances (e.g., autoantibodies) from the blood, it is considered

> a

> > viable immune therapy. The method has been used to treat certain

> brain

> > disorders, for example Rasmussen's encephalitis (RE) and

> > obsessive-compulsive disorder (OCD), in which autoimmunity has been

> > implicated as a basis of the disorder. Plasmapheresis produced

> positive

> > responses in patients with these disorders, and the responses were

> much

> > better with plasmapheresis when compared to the IVIG treatment. In

> each

> > case, the benefit to the patient was associated with the lowering

> of

> > the anti-neuronal antibody titers. Since autistic patients also

> have

> > positive titers of brain autoantibodies, they should also respond

> to

> > plasmapheresis. Although this treatment has long been suggested

> for use

> > in autism (V. Singh, 1997), plasmapheresis has thus far not been

> tried

> > in patients with this disorder.

> >

> > Conclusion

> >

> > The evidence is rapidly accumulating to suggest that autism is an

> > autoimmune disorder. The autoimmune response is most likely

> directed

> > against the brain myelin, perhaps secondary to a viral infection.

> > Measles virus is a candidate but other possibilities remain to be

> > explored. More importantly, the patients respond to treatment with

> > immune therapies. Therefore, I conclude that autoimmunity

> offersstrong

> > prospects for drug discovery and therapy for autism. Naturally, it

> > deserves prompt attention from all those who want to help people

> with

> > autism.

> >

> > Selected Reading

> >

> > Singh, V. K., " Plasma Increase of Interleukin-12 and Interferon-

> gamma:

> > Pathological Significance in Autism " (Journal of Neuroimmunology,

> vol.

> > 66, pp. 143-145 [1996]).

> >

> > Singh, V. K., " Immunotherapy for Brain Diseases and Mental

> Illnesses, "

> > (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

> >

> > Singh, V. K., " Serological Association of Measles Virus and Human

> > Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

> Immunology

> > and Immunopathology, vol. 89, pp. 105-108 [1998]).

> >

> > Singh, V. K., " Autoimmunity and Neurologic Disorders " (Latitudes,

> vol.

> > 4, pp. 5-11 [1999]).

> >

> > Dr. Singh received his doctorate from the University of British

> > Columbia, Vancouver, Canada. His post-doctoral fellowship was

> completed

> > in neurochemistry and neuroimmunology. Spanning over twenty years'

> > experience in neurobiology and immunology research, Dr. Singh

> studied

> > brain diseases, particularly infantile autism and Alzheimer's

> disease.

> > Having authored over a hundred scientific publications, he is both

> a

> > pioneer and an international authority on autoimmunity in autism.

> Dr.

> > Singh is a member of the American Association for the Advancement

> of

> > Sciences, the American Association of Immunologists, and the New

> York

> > Academy of Sciences. He is listed in American Men and Women in

> Science

> > (United States, R. R. Bowker, publisher) and The International

> Who's

> > Who of Intellectuals (Cambridge, England, International

> Biographical

> > Centre).

> >

> > For further information, please contact Dr. Vijendra Singh, Ph.D.,

> at

> > the Biotechnology Center, Department of Biology, Utah State

> University,

> > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> > singhvk@].

> >

> > Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,

> vol. 1,

> > number 2, December 1999.

> >

> >

> >

> > Links

> >

> > " Autoimmunity and Neurological Disorders, " interview with V. K.

> Singh in

> > Latitudes, newsletter of the Association for

> > Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,

> vol. 4,

> > no. 2, Spring 1999, by Sheila

> > : http://lib.tcu.edu/www/staff/lruede/latitudes

> >

> > " V. K. Singh: Selected Research on Autism, "

> http://www.gti.net/truegrit/

> > : Findings in Immunology

> >

> > " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease, "

> > (http://lib.tcu.edu/www/staff/lruede/alzheimers)

> >

> >

> >

> >

> > > __________________________________________________

> > > Correo Yahoo!

> > > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > > Regístrate ya - http://correo.espanol.yahoo.com/

> > >

> >

>

[Guest guest]

particularly because the Hopkinson findings are brain auto-immunity.

xx Sally

natasa778 wrote:

>

> ... I find it very odd that his findings and suggestions have not been

> explored by DAN! and others to greater extent!

>

> I have saved the text below a while ago, someone brought up

> discussion on one of the treatments..

>

> here is a bit more on his work:

> http://www.latitude s.org/articles/ singh_neuro_ ts.html

>

>

> 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

>

> Autism is an early-onset biological disorder that causes severe

> deficits of higher mental functions, as well as behavioral

> manifestations. There is no single, clear-cut cause and no complete

> cure for autism. Causally speaking, immune factors, neuro-chemical

> factors, genetic susceptibility factors and environmental factors

> (such as microbial infections and chemical toxicity) have been

> implicated. I view autism as a very complex, multifactorial disorder.

> In this article, I will attempt to describe succinctly the role of

> autoimmune etiology and immune therapy for autism.

>

> As a neuroimmunologist, I have been interested in the immunology of

> the nervous system, i.e., the immune basis and immune therapy for

> brain diseases and mental illnesses. I have studied autism as an

> autoimmune disorder for over fifteen years. As a result, 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. I

> recently postulated a " Neuroautoimmunity Model of Autism " which I

> discussed at two recent conferences: first, the Biomedical Treatments

> for Autism and PDD Conference held in Orlando, Florida (May, 1999);

> and second, the Neuro-Immune Dysfunction Syndromes (NIDS) Conference

> held in Bethesda, land (June, 1999). Briefly, I hypothesized that

> an autoimmune reaction to brain structures, in particular the myelin

> sheath, plays a critical role in causing the neurological impairments

> of patients with autism. I 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.

>

> I believe that autism can be treated successfully using some of the

> therapies proven effective in treating other autoimmune diseases. I am

> exploring specifically the role of autoimmune factors, (e.g., viruses,

> autoantibodies, T cells, and cytokines) because they serve as the

> prime targets of therapy with immune-modulating agents. I emphasize

> the need to focus on immunotherapies, and I urge doctors toexamine

> autoimmunity as a novel target on which to focus in treating autistic

> patients. There is enormous potential for restoring brain function in

> autistic children and adults through immunology.

>

> Autoimmune Etiology in Autism

>

> A disease is commonly 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. While some

> of the key features are listed below, I will focus more on the current

> research relating to three topics: viral studies; autoimmune testing;

> and autoimmune therapy. 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, extended haplotypes, etc.

>

> 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 respond well to immune therapies.

>

> Viral Studies in Autism

>

> Viruses have been linked to autism, but this relationship is far from

> fully explored. 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 was 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 never been investigated, I think this

> is due to a defect in T lymphocytes- these agents of immune response

> are not functioning properly in these children. In an unpublished

> pilot study, I found that the RV-induced lymphocyte proliferation

> response in autistic children was only one-fourth of the response in

> normal children, which clearly suggests a defect of T cell-mediated

> immunity (a defense mechanism that helps fight virus infections).

>

> 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. A few

> years ago I and coworkers conducted a study of IgG antibodies to CMV;

> we found no statistical difference between autistic children and

> normal children (V. Singh, D. Schubert and R. Warren, 1992;

> unpublished data). Simply put, this means that CMV is probably not

> related to autism.

>

> More recently, I conducted a study of measles virus (MV) and human

> herpesvirus- 6 (HHV-6) in autism. This was done by two types of

> laboratory analysis: (a) virus antibody levels of MV and HHV-6; and

> ( brain autoantibody titers in the same samples as those assayed for

> virus antibodies. 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 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 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.

>

> Testing for Autoimmunity in Autism

>

> Recent advances have clearly shown that autoimmunity plays a key role

> in the pathogenesis of autism. Since the brain is the affected organ

> in autism, the autoimmune response will be directed against this

> organ. This response is commonly identified by certain autoimmune

> factors which I have identified in autistic children. The list

> includes brain-specific autoantibodies, viral antibodies, cytokine

> profile or immune activation markers, as well as antinuclear

> antibodies. Collectively, they are essential for identifying a

> brain-specific autoimmune response, which can afterward be treated

> with immune therapy. By performing blood tests we can determine if a

> patient shows autoimmunity to brain tissues, if he or she is a

> candidate for experimental immune therapy, and if the response to

> therapy is effective. Therefore, this type of immune evaluation is

> very important in helping children with autism.

>

> Brain autoantibodies: this test detects antibodies to two brain

> proteins, namely 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. It is, however,

> recommended that the two markers be tested simultaneously.

>

> Cytokine profile: 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: this test 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: this test assays for antinuclear antibodies

> (ANA). They are non-specific antibodies but are often present in

> patients with autoimmune diseases. Approximately one-third of autistic

> children tested have positive titers of ANA (V. Singh, 1992;

> unpublished data).

>

> Immunotherapy in Autism

>

> The aforementioned laboratory findings clearly point to an autoimmune

> pathogenic mechanism in autism. The idea that autism is an autoimmune

> disorder is further strengthened by the fact that autistic patients

> respond well to treatment with immune modulating drugs. Immune

> interventions can produce immune modulation-a state of suppression or

> stimulation. Depending on the nature of the immune abnormality, 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. Immune therapy should always be done in consultation

> with physicians. The following immune interventions can be used:

>

> Steroid therapy: steroids such as Prednisone and/or ACTH

> (adrenocorticotropi n hormone) are commonly used as anti-inflammatory

> and/or immunosuppressive drugs for treating patients with autoimmune

> diseases, inflammatory diseases, etc. In autism, however, there is

> only one study that showed improvement of autistic-like symptoms in

> children when they were treated with an ACTH analogue. This result

> indicated that steroids are potentially useful in alleviating clinical

> symptoms of autism. Steroids are the first course of treatment for

> patients with autoimmune diseases and infantile spasm; however, their

> efficacy has not been evaluated in autism.

>

> Intraveneous immunoglobulin (IVIG): this type of treatment has been

> used to treat children with autism. Open-label trials of both low-dose

> and high-dose IVIG have shown that most but not all autistic children

> respond favorably to this treatment. My collaborators and I recently

> found that the high-dose IVIG was better than the low-dose IVIG (J.

> Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> International Symposium on Autism, Netherlands, December 28-30, 1999).

> Clinically, children so treated have shown improvements in language,

> communication, social interaction and attention span. In a

> double-blind study, (V. Singh, 1997; unpublished data) the IVIG

> treatment was found to decrease brain autoantibody titers in five

> patients (they were positive pre-therapy but became virtually negative

> post-therapy) who also showed clinical improvement of autistic

> characteristics. In spite of the success of IVIG, this treatment is

> not for everyone. Before this treatment is administered, a proper

> immune evaluation is highly recommended to assess the nature of the

> immune problem.

>

> Oral tolerance with autoantigens: this treatment is a means of

> inducing immune suppression by feeding patients autoantigen. I have

> shown that the candidate autoantigen in autism appeared to be a myelin

> basic protein (MBP); this suggested that the MBP-containing myelin

> products can be used to treat autistic patients. Indeed, one such

> product known as Sphingolin has been used with success. Recently, the

> parents, school psychologists, and other professionals have

> anecdotally reported tremendous improvements of autistic symptoms in

> their children. These reports are undoubtedly quite encouraging and

> promising, but a well-designed clinical trial is warranted.

>

> Plasmapheresis: although it is not commonly recommended, this

> procedure is used for treating patients with infections, autoimmune

> diseases, immune complex diseases, etc. Because this method removes

> harmful substances (e.g., autoantibodies) from the blood, it is

> considered a viable immune therapy. The method has been used to treat

> certain brain disorders, for example Rasmussen's encephalitis (RE) and

> obsessive-compulsiv e disorder (OCD), in which autoimmunity has been

> implicated as a basis of the disorder. Plasmapheresis produced

> positive responses in patients with these disorders, and the responses

> were much better with plasmapheresis when compared to the IVIG

> treatment. In each case, the benefit to the patient was associated

> with the lowering of the anti-neuronal antibody titers. Since autistic

> patients also have positive titers of brain autoantibodies, they

> should also respond to plasmapheresis. Although this treatment has

> long been suggested for use in autism (V. Singh, 1997), plasmapheresis

> has thus far not been tried in patients with this disorder.

>

> Conclusion

>

> The evidence is rapidly accumulating to suggest that autism is an

> autoimmune disorder. The autoimmune response is most likely directed

> against the brain myelin, perhaps secondary to a viral infection.

> Measles virus is a candidate but other possibilities remain to be

> explored. More importantly, the patients respond to treatment with

> immune therapies. Therefore, I conclude that autoimmunity offersstrong

> prospects for drug discovery and therapy for autism. Naturally, it

> deserves prompt attention from all those who want to help people with

> autism.

>

> Selected Reading

>

> Singh, V. K., " Plasma Increase of Interleukin- 12 and

> Interferon-gamma: Pathological Significance in Autism " (Journal of

> Neuroimmunology, vol. 66, pp. 143-145 [1996]).

>

> Singh, V. K., " Immunotherapy for Brain Diseases and Mental Illnesses, "

> (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

>

> Singh, V. K., " Serological Association of Measles Virus and Human

> Herpesvirus- 6 With Brain Autoantibodies in Autism " (Clinical

> Immunology and Immunopathology, vol. 89, pp. 105-108 [1998]).

>

> Singh, V. K., " Autoimmunity and Neurologic Disorders " (Latitudes, vol.

> 4, pp. 5-11 [1999]).

>

> Dr. Singh received his doctorate from the University of British

> Columbia, Vancouver, Canada. His post-doctoral fellowship was

> completed in neurochemistry and neuroimmunology. Spanning over twenty

> years' experience in neurobiology and immunology research, Dr. Singh

> studied brain diseases, particularly infantile autism and Alzheimer's

> disease. Having authored over a hundred scientific publications, he is

> both a pioneer and an international authority on autoimmunity in

> autism. Dr. Singh is a member of the American Association for the

> Advancement of Sciences, the American Association of Immunologists,

> and the New York Academy of Sciences. He is listed in American Men and

> Women in Science (United States, R. R. Bowker, publisher) and The

> International Who's Who of Intellectuals (Cambridge, England,

> International Biographical Centre).

>

> For further information, please contact Dr. Vijendra Singh, Ph.D., at

> the Biotechnology Center, Department of Biology, Utah State

> University, 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> singhvkbiology (DOT) usu.edu].

>

> Reprinted from AAPN, The Autism Autoimmunity Project Newsletter, vol.

> 1, number 2, December 1999.

>

>

>

> Links

>

> " Autoimmunity and Neurological Disorders, " interview with V. K. Singh

> in Latitudes, newsletter of the Association for

> Comprehensive NeuroTherapy, http://www.latitude s.org/index. html,

> vol. 4, no. 2, Spring 1999, by Sheila

> : http://lib.tcu. edu/www/staff/ lruede/latitudes

>

> " V. K. Singh: Selected Research on Autism, " http://www.gti.

> net/truegrit/ : Findings in Immunology

>

> " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease, "

> (http://lib. tcu.edu/www/ staff/lruede/ alzheimers)

>

>

>

>

> > ____________ _________ _________ _________ _________ __

> > Correo Yahoo!

> > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > Regístrate ya - http://correo. espanol.yahoo. com/

> >

>

>

> ------------------------------------------------------------------------

>

> No virus found in this incoming message.

> Checked by AVG Free Edition.

> Version: 7.5.485 / Virus Database: 269.13.16/1004 - Release Date: 12/09/2007

17:22

>

[Guest guest]

I'd be very worried about vCJD with this product...

Margaret

> >

> > ... I find it very odd that his findings and suggestions have not

> been

> > explored by DAN! and others to greater extent!

> >

> > I have saved the text below a while ago, someone brought up

> discussion

> > on one of the treatments..

> >

> > here is a bit more on his work:

> > http://www.latitudes.org/articles/singh_neuro_ts.html

> >

> >

> > 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

> >

> > Autism is an early-onset biological disorder that causes severe

> > deficits of higher mental functions, as well as behavioral

> > manifestations. There is no single, clear-cut cause and no

complete

> > cure for autism. Causally speaking, immune factors, neuro-chemical

> > factors, genetic susceptibility factors and environmental factors

> (such

> > as microbial infections and chemical toxicity) have been

implicated. I

> > view autism as a very complex, multifactorial disorder. In this

> > article, I will attempt to describe succinctly the role of

autoimmune

> > etiology and immune therapy for autism.

> >

> > As a neuroimmunologist, I have been interested in the immunology

of

> the

> > nervous system, i.e., the immune basis and immune therapy for

brain

> > diseases and mental illnesses. I have studied autism as an

autoimmune

> > disorder for over fifteen years. As a result, 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. I recently postulated a

> > " Neuroautoimmunity Model of Autism " which I discussed at two

recent

> > conferences: first, the Biomedical Treatments for Autism and PDD

> > Conference held in Orlando, Florida (May, 1999); and second, the

> > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

Bethesda,

> > land (June, 1999). Briefly, I hypothesized that an autoimmune

> > reaction to brain structures, in particular the myelin sheath,

plays a

> > critical role in causing the neurological impairments of patients

with

> > autism. I 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.

> >

> > I believe that autism can be treated successfully using some of

the

> > therapies proven effective in treating other autoimmune diseases.

I am

> > exploring specifically the role of autoimmune factors, (e.g.,

viruses,

> > autoantibodies, T cells, and cytokines) because they serve as the

> prime

> > targets of therapy with immune-modulating agents. I emphasize the

need

> > to focus on immunotherapies, and I urge doctors toexamine

autoimmunity

> > as a novel target on which to focus in treating autistic patients.

> > There is enormous potential for restoring brain function in

autistic

> > children and adults through immunology.

> >

> > Autoimmune Etiology in Autism

> >

> > A disease is commonly 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. While

some

> > of the key features are listed below, I will focus more on the

current

> > research relating to three topics: viral studies; autoimmune

testing;

> > and autoimmune therapy. 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, extended haplotypes, etc.

> >

> > 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 respond well to immune therapies.

> >

> > Viral Studies in Autism

> >

> > Viruses have been linked to autism, but this relationship is far

from

> > fully explored. 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 was 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 never been investigated, I think

this

> > is due to a defect in T lymphocytes-these agents of immune

response

> are

> > not functioning properly in these children. In an unpublished

pilot

> > study, I found that the RV-induced lymphocyte proliferation

response

> in

> > autistic children was only one-fourth of the response in normal

> > children, which clearly suggests a defect of T cell-mediated

immunity

> > (a defense mechanism that helps fight virus infections).

> >

> > 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. A few

years

> > ago I and coworkers conducted a study of IgG antibodies to CMV; we

> > found no statistical difference between autistic children and

normal

> > children (V. Singh, D. Schubert and R. Warren, 1992; unpublished

> data).

> > Simply put, this means that CMV is probably not related to autism.

> >

> > More recently, I conducted a study of measles virus (MV) and human

> > herpesvirus-6 (HHV-6) in autism. This was done by two types of

> > laboratory analysis: (a) virus antibody levels of MV and HHV-6;

and

> (

> > brain autoantibody titers in the same samples as those assayed for

> > virus antibodies. 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

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 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.

> >

> > Testing for Autoimmunity in Autism

> >

> > Recent advances have clearly shown that autoimmunity plays a key

role

> > in the pathogenesis of autism. Since the brain is the affected

organ

> in

> > autism, the autoimmune response will be directed against this

organ.

> > This response is commonly identified by certain autoimmune factors

> > which I have identified in autistic children. The list includes

> > brain-specific autoantibodies, viral antibodies, cytokine

profile or

> > immune activation markers, as well as antinuclear antibodies.

> > Collectively, they are essential for identifying a brain-specific

> > autoimmune response, which can afterward be treated with immune

> > therapy. By performing blood tests we can determine if a patient

shows

> > autoimmunity to brain tissues, if he or she is a candidate for

> > experimental immune therapy, and if the response to therapy is

> > effective. Therefore, this type of immune evaluation is very

important

> > in helping children with autism.

> >

> > Brain autoantibodies: this test detects antibodies to two brain

> > proteins, namely 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. It is, however, recommended that the two

> > markers be tested simultaneously.

> >

> > Cytokine profile: 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: this test 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: this test assays for antinuclear

antibodies

> > (ANA). They are non-specific antibodies but are often present in

> > patients with autoimmune diseases. Approximately one-third of

> autistic

> > children tested have positive titers of ANA (V. Singh, 1992;

> > unpublished data).

> >

> > Immunotherapy in Autism

> >

> > The aforementioned laboratory findings clearly point to an

autoimmune

> > pathogenic mechanism in autism. The idea that autism is an

autoimmune

> > disorder is further strengthened by the fact that autistic

patients

> > respond well to treatment with immune modulating drugs. Immune

> > interventions can produce immune modulation-a state of

suppression or

> > stimulation. Depending on the nature of the immune abnormality,

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. Immune therapy should always be done in

consultation

> > with physicians. The following immune interventions can be used:

> >

> > Steroid therapy: steroids such as Prednisone and/or ACTH

> > (adrenocorticotropin hormone) are commonly used as anti-

inflammatory

> > and/or immunosuppressive drugs for treating patients with

autoimmune

> > diseases, inflammatory diseases, etc. In autism, however, there

is

> only

> > one study that showed improvement of autistic-like symptoms in

> children

> > when they were treated with an ACTH analogue. This result

indicated

> > that steroids are potentially useful in alleviating clinical

symptoms

> > of autism. Steroids are the first course of treatment for

patients

> with

> > autoimmune diseases and infantile spasm; however, their efficacy

has

> > not been evaluated in autism.

> >

> > Intraveneous immunoglobulin (IVIG): this type of treatment has

been

> > used to treat children with autism. Open-label trials of both

> low-dose

> > and high-dose IVIG have shown that most but not all autistic

children

> > respond favorably to this treatment. My collaborators and I

recently

> > found that the high-dose IVIG was better than the low-dose IVIG

(J.

> > Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> > International Symposium on Autism, Netherlands, December 28-30,

> 1999).

> > Clinically, children so treated have shown improvements in

language,

> > communication, social interaction and attention span. In a

> double-blind

> > study, (V. Singh, 1997; unpublished data) the IVIG treatment was

> found

> > to decrease brain autoantibody titers in five patients (they were

> > positive pre-therapy but became virtually negative post-therapy)

who

> > also showed clinical improvement of autistic characteristics. In

> spite

> > of the success of IVIG, this treatment is not for everyone.

Before

> this

> > treatment is administered, a proper immune evaluation is highly

> > recommended to assess the nature of the immune problem.

> >

> > Oral tolerance with autoantigens: this treatment is a means of

> inducing

> > immune suppression by feeding patients autoantigen. I have shown

that

> > the candidate autoantigen in autism appeared to be a myelin basic

> > protein (MBP); this suggested that the MBP-containing myelin

products

> > can be used to treat autistic patients. Indeed, one such product

known

> > as Sphingolin has been used with success. Recently, the parents,

> school

> > psychologists, and other professionals have anecdotally reported

> > tremendous improvements of autistic symptoms in their children.

These

> > reports are undoubtedly quite encouraging and promising, but a

> > well-designed clinical trial is warranted.

> >

> > Plasmapheresis: although it is not commonly recommended, this

> procedure

> > is used for treating patients with infections, autoimmune

diseases,

> > immune complex diseases, etc. Because this method removes harmful

> > substances (e.g., autoantibodies) from the blood, it is

considered a

> > viable immune therapy. The method has been used to treat certain

> brain

> > disorders, for example Rasmussen's encephalitis (RE) and

> > obsessive-compulsive disorder (OCD), in which autoimmunity has

been

> > implicated as a basis of the disorder. Plasmapheresis produced

> positive

> > responses in patients with these disorders, and the responses

were

> much

> > better with plasmapheresis when compared to the IVIG treatment.

In

> each

> > case, the benefit to the patient was associated with the

lowering of

> > the anti-neuronal antibody titers. Since autistic patients also

have

> > positive titers of brain autoantibodies, they should also

respond to

> > plasmapheresis. Although this treatment has long been suggested

for

> use

> > in autism (V. Singh, 1997), plasmapheresis has thus far not been

> tried

> > in patients with this disorder.

> >

> > Conclusion

> >

> > The evidence is rapidly accumulating to suggest that autism is an

> > autoimmune disorder. The autoimmune response is most likely

directed

> > against the brain myelin, perhaps secondary to a viral infection.

> > Measles virus is a candidate but other possibilities remain to be

> > explored. More importantly, the patients respond to treatment with

> > immune therapies. Therefore, I conclude that autoimmunity

offersstrong

> > prospects for drug discovery and therapy for autism. Naturally, it

> > deserves prompt attention from all those who want to help people

with

> > autism.

> >

> > Selected Reading

> >

> > Singh, V. K., " Plasma Increase of Interleukin-12 and Interferon-

gamma:

> > Pathological Significance in Autism " (Journal of Neuroimmunology,

vol.

> > 66, pp. 143-145 [1996]).

> >

> > Singh, V. K., " Immunotherapy for Brain Diseases and Mental

Illnesses, "

> > (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

> >

> > Singh, V. K., " Serological Association of Measles Virus and Human

> > Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

> Immunology

> > and Immunopathology, vol. 89, pp. 105-108 [1998]).

> >

> > Singh, V. K., " Autoimmunity and Neurologic Disorders " (Latitudes,

vol.

> > 4, pp. 5-11 [1999]).

> >

> > Dr. Singh received his doctorate from the University of British

> > Columbia, Vancouver, Canada. His post-doctoral fellowship was

> completed

> > in neurochemistry and neuroimmunology. Spanning over twenty years'

> > experience in neurobiology and immunology research, Dr. Singh

studied

> > brain diseases, particularly infantile autism and Alzheimer's

disease.

> > Having authored over a hundred scientific publications, he is

both a

> > pioneer and an international authority on autoimmunity in autism.

Dr.

> > Singh is a member of the American Association for the Advancement

of

> > Sciences, the American Association of Immunologists, and the New

York

> > Academy of Sciences. He is listed in American Men and Women in

Science

> > (United States, R. R. Bowker, publisher) and The International

Who's

> > Who of Intellectuals (Cambridge, England, International

Biographical

> > Centre).

> >

> > For further information, please contact Dr. Vijendra Singh,

Ph.D., at

> > the Biotechnology Center, Department of Biology, Utah State

> University,

> > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> > singhvk@].

> >

> > Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,

vol.

> 1,

> > number 2, December 1999.

> >

> >

> >

> > Links

> >

> > " Autoimmunity and Neurological Disorders, " interview with V. K.

Singh

> in

> > Latitudes, newsletter of the Association for

> > Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,

vol.

> 4,

> > no. 2, Spring 1999, by Sheila

> > : http://lib.tcu.edu/www/staff/lruede/latitudes

> >

> > " V. K. Singh: Selected Research on Autism, "

> http://www.gti.net/truegrit/

> > : Findings in Immunology

> >

> > " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease, "

> > (http://lib.tcu.edu/www/staff/lruede/alzheimers)

> >

> >

> >

> >

> > > __________________________________________________

> > > Correo Yahoo!

> > > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > > Regístrate ya - http://correo.espanol.yahoo.com/

> > >

> >

>

[Guest guest]

Maybe he didnt pay a DAN membership fee?

I dont agree with all DAN is about, as there is so much missing.

Maybe Dr Singh is of this ilk as well and is outside the " pale " of

the DAN movement??

>

> ... I find it very odd that his findings and suggestions have not

been

> explored by DAN! and others to greater extent!

>

> I have saved the text below a while ago, someone brought up

discussion

> on one of the treatments..

>

> here is a bit more on his work:

> http://www.latitudes.org/articles/singh_neuro_ts.html

>

>

> 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

>

> Autism is an early-onset biological disorder that causes severe

> deficits of higher mental functions, as well as behavioral

> manifestations. There is no single, clear-cut cause and no

complete

> cure for autism. Causally speaking, immune factors, neuro-chemical

> factors, genetic susceptibility factors and environmental factors

(such

> as microbial infections and chemical toxicity) have been

implicated. I

> view autism as a very complex, multifactorial disorder. In this

> article, I will attempt to describe succinctly the role of

autoimmune

> etiology and immune therapy for autism.

>

> As a neuroimmunologist, I have been interested in the immunology

of the

> nervous system, i.e., the immune basis and immune therapy for

brain

> diseases and mental illnesses. I have studied autism as an

autoimmune

> disorder for over fifteen years. As a result, 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. I recently postulated a

> " Neuroautoimmunity Model of Autism " which I discussed at two

recent

> conferences: first, the Biomedical Treatments for Autism and PDD

> Conference held in Orlando, Florida (May, 1999); and second, the

> Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

Bethesda,

> land (June, 1999). Briefly, I hypothesized that an autoimmune

> reaction to brain structures, in particular the myelin sheath,

plays a

> critical role in causing the neurological impairments of patients

with

> autism. I 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.

>

> I believe that autism can be treated successfully using some of

the

> therapies proven effective in treating other autoimmune diseases.

I am

> exploring specifically the role of autoimmune factors, (e.g.,

viruses,

> autoantibodies, T cells, and cytokines) because they serve as the

prime

> targets of therapy with immune-modulating agents. I emphasize the

need

> to focus on immunotherapies, and I urge doctors toexamine

autoimmunity

> as a novel target on which to focus in treating autistic patients.

> There is enormous potential for restoring brain function in

autistic

> children and adults through immunology.

>

> Autoimmune Etiology in Autism

>

> A disease is commonly 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. While

some

> of the key features are listed below, I will focus more on the

current

> research relating to three topics: viral studies; autoimmune

testing;

> and autoimmune therapy. 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, extended haplotypes, etc.

>

> 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 respond well to immune therapies.

>

> Viral Studies in Autism

>

> Viruses have been linked to autism, but this relationship is far

from

> fully explored. 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 was 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 never been investigated, I think

this

> is due to a defect in T lymphocytes-these agents of immune

response are

> not functioning properly in these children. In an unpublished

pilot

> study, I found that the RV-induced lymphocyte proliferation

response in

> autistic children was only one-fourth of the response in normal

> children, which clearly suggests a defect of T cell-mediated

immunity

> (a defense mechanism that helps fight virus infections).

>

> 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. A few

years

> ago I and coworkers conducted a study of IgG antibodies to CMV; we

> found no statistical difference between autistic children and

normal

> children (V. Singh, D. Schubert and R. Warren, 1992; unpublished

data).

> Simply put, this means that CMV is probably not related to autism.

>

> More recently, I conducted a study of measles virus (MV) and human

> herpesvirus-6 (HHV-6) in autism. This was done by two types of

> laboratory analysis: (a) virus antibody levels of MV and HHV-6;

and (

> brain autoantibody titers in the same samples as those assayed for

> virus antibodies. 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

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 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.

>

> Testing for Autoimmunity in Autism

>

> Recent advances have clearly shown that autoimmunity plays a key

role

> in the pathogenesis of autism. Since the brain is the affected

organ in

> autism, the autoimmune response will be directed against this

organ.

> This response is commonly identified by certain autoimmune factors

> which I have identified in autistic children. The list includes

> brain-specific autoantibodies, viral antibodies, cytokine profile

or

> immune activation markers, as well as antinuclear antibodies.

> Collectively, they are essential for identifying a brain-specific

> autoimmune response, which can afterward be treated with immune

> therapy. By performing blood tests we can determine if a patient

shows

> autoimmunity to brain tissues, if he or she is a candidate for

> experimental immune therapy, and if the response to therapy is

> effective. Therefore, this type of immune evaluation is very

important

> in helping children with autism.

>

> Brain autoantibodies: this test detects antibodies to two brain

> proteins, namely 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. It is, however, recommended that the two

> markers be tested simultaneously.

>

> Cytokine profile: 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: this test 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: this test assays for antinuclear

antibodies

> (ANA). They are non-specific antibodies but are often present in

> patients with autoimmune diseases. Approximately one-third of

autistic

> children tested have positive titers of ANA (V. Singh, 1992;

> unpublished data).

>

> Immunotherapy in Autism

>

> The aforementioned laboratory findings clearly point to an

autoimmune

> pathogenic mechanism in autism. The idea that autism is an

autoimmune

> disorder is further strengthened by the fact that autistic

patients

> respond well to treatment with immune modulating drugs. Immune

> interventions can produce immune modulation-a state of suppression

or

> stimulation. Depending on the nature of the immune abnormality,

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. Immune therapy should always be done in

consultation

> with physicians. The following immune interventions can be used:

>

> Steroid therapy: steroids such as Prednisone and/or ACTH

> (adrenocorticotropin hormone) are commonly used as anti-

inflammatory

> and/or immunosuppressive drugs for treating patients with

autoimmune

> diseases, inflammatory diseases, etc. In autism, however, there

is only

> one study that showed improvement of autistic-like symptoms in

children

> when they were treated with an ACTH analogue. This result

indicated

> that steroids are potentially useful in alleviating clinical

symptoms

> of autism. Steroids are the first course of treatment for

patients with

> autoimmune diseases and infantile spasm; however, their efficacy

has

> not been evaluated in autism.

>

> Intraveneous immunoglobulin (IVIG): this type of treatment has

been

> used to treat children with autism. Open-label trials of both low-

dose

> and high-dose IVIG have shown that most but not all autistic

children

> respond favorably to this treatment. My collaborators and I

recently

> found that the high-dose IVIG was better than the low-dose IVIG

(J.

> Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> International Symposium on Autism, Netherlands, December 28-30,

1999).

> Clinically, children so treated have shown improvements in

language,

> communication, social interaction and attention span. In a double-

blind

> study, (V. Singh, 1997; unpublished data) the IVIG treatment was

found

> to decrease brain autoantibody titers in five patients (they were

> positive pre-therapy but became virtually negative post-therapy)

who

> also showed clinical improvement of autistic characteristics. In

spite

> of the success of IVIG, this treatment is not for everyone.

Before this

> treatment is administered, a proper immune evaluation is highly

> recommended to assess the nature of the immune problem.

>

> Oral tolerance with autoantigens: this treatment is a means of

inducing

> immune suppression by feeding patients autoantigen. I have shown

that

> the candidate autoantigen in autism appeared to be a myelin basic

> protein (MBP); this suggested that the MBP-containing myelin

products

> can be used to treat autistic patients. Indeed, one such product

known

> as Sphingolin has been used with success. Recently, the parents,

school

> psychologists, and other professionals have anecdotally reported

> tremendous improvements of autistic symptoms in their children.

These

> reports are undoubtedly quite encouraging and promising, but a

> well-designed clinical trial is warranted.

>

> Plasmapheresis: although it is not commonly recommended, this

procedure

> is used for treating patients with infections, autoimmune

diseases,

> immune complex diseases, etc. Because this method removes harmful

> substances (e.g., autoantibodies) from the blood, it is

considered a

> viable immune therapy. The method has been used to treat certain

brain

> disorders, for example Rasmussen's encephalitis (RE) and

> obsessive-compulsive disorder (OCD), in which autoimmunity has

been

> implicated as a basis of the disorder. Plasmapheresis produced

positive

> responses in patients with these disorders, and the responses

were much

> better with plasmapheresis when compared to the IVIG treatment.

In each

> case, the benefit to the patient was associated with the lowering

of

> the anti-neuronal antibody titers. Since autistic patients also

have

> positive titers of brain autoantibodies, they should also respond

to

> plasmapheresis. Although this treatment has long been suggested

for use

> in autism (V. Singh, 1997), plasmapheresis has thus far not been

tried

> in patients with this disorder.

>

> Conclusion

>

> The evidence is rapidly accumulating to suggest that autism is an

> autoimmune disorder. The autoimmune response is most likely

directed

> against the brain myelin, perhaps secondary to a viral infection.

> Measles virus is a candidate but other possibilities remain to be

> explored. More importantly, the patients respond to treatment with

> immune therapies. Therefore, I conclude that autoimmunity

offersstrong

> prospects for drug discovery and therapy for autism. Naturally, it

> deserves prompt attention from all those who want to help people

with

> autism.

>

> Selected Reading

>

> Singh, V. K., " Plasma Increase of Interleukin-12 and Interferon-

gamma:

> Pathological Significance in Autism " (Journal of Neuroimmunology,

vol.

> 66, pp. 143-145 [1996]).

>

> Singh, V. K., " Immunotherapy for Brain Diseases and Mental

Illnesses, "

> (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

>

> Singh, V. K., " Serological Association of Measles Virus and Human

> Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

Immunology

> and Immunopathology, vol. 89, pp. 105-108 [1998]).

>

> Singh, V. K., " Autoimmunity and Neurologic Disorders " (Latitudes,

vol.

> 4, pp. 5-11 [1999]).

>

> Dr. Singh received his doctorate from the University of British

> Columbia, Vancouver, Canada. His post-doctoral fellowship was

completed

> in neurochemistry and neuroimmunology. Spanning over twenty years'

> experience in neurobiology and immunology research, Dr. Singh

studied

> brain diseases, particularly infantile autism and Alzheimer's

disease.

> Having authored over a hundred scientific publications, he is both

a

> pioneer and an international authority on autoimmunity in autism.

Dr.

> Singh is a member of the American Association for the Advancement

of

> Sciences, the American Association of Immunologists, and the New

York

> Academy of Sciences. He is listed in American Men and Women in

Science

> (United States, R. R. Bowker, publisher) and The International

Who's

> Who of Intellectuals (Cambridge, England, International

Biographical

> Centre).

>

> For further information, please contact Dr. Vijendra Singh, Ph.D.,

at

> the Biotechnology Center, Department of Biology, Utah State

University,

> 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> singhvk@...].

>

> Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,

vol. 1,

> number 2, December 1999.

>

>

>

> Links

>

> " Autoimmunity and Neurological Disorders, " interview with V. K.

Singh in

> Latitudes, newsletter of the Association for

> Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,

vol. 4,

> no. 2, Spring 1999, by Sheila

> : http://lib.tcu.edu/www/staff/lruede/latitudes

>

> " V. K. Singh: Selected Research on Autism, "

http://www.gti.net/truegrit/

> : Findings in Immunology

>

> " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease, "

> (http://lib.tcu.edu/www/staff/lruede/alzheimers)

>

>

>

>

> > __________________________________________________

> > Correo Yahoo!

> > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > Regístrate ya - http://correo.espanol.yahoo.com/

> >

>

[Guest guest]

No, I think they have included Dr. Singh and his research in the dan! movement. But like all single theories, Dr. Singh's fell by the wayside. It isn't that it can't be significant for a small subset but doesn't explain or help ameliorate the symptoms of the vast majority of ASD kids, but it was an important piece and I think Dr. McCandless, at least in part, based her laboratory testing on some of his findings, as did other Dan! drs.

Again this is old news and research but not necessarily inconsequential for someone's specific child, for whom which the improvement, if needed, would prove invaluable. Read everything and apply what seems pertinent for your particular child. But anytime someone starts talking about one treatment for all kids you can pretty well know that it's irrelevant for the majority, invaluable for a few.

It's interesting to me how the various treatments and their originators are rarely satisfied that they help some kids, they're constantly looking to expand the number of children it helps, a glorious goal, but ASD does not work that way.

Re: Autism tests and treatments - recommened by Dr Singh

Maybe he didnt pay a DAN membership fee?I dont agree with all DAN is about, as there is so much missing. Maybe Dr Singh is of this ilk as well and is outside the "pale" of the DAN movement??>> ... I find it very odd that his findings and suggestions have not been> explored by DAN! and others to greater extent!> > I have saved the text below a while ago, someone brought up discussion> on one of the treatments..> > here is a bit more on his work:> http://www.latitudes.org/articles/singh_neuro_ts.html> > > 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> > Autism is an early-onset biological disorder that causes severe > deficits of higher mental functions, as well as behavioral > manifestations. There is no single, clear-cut cause and no complete > cure for autism. Causally speaking, immune factors, neuro-chemical > factors, genetic susceptibility factors and environmental factors (such > as microbial infections and chemical toxicity) have been implicated. I > view autism as a very complex, multifactorial disorder. In this > article, I will attempt to describe succinctly the role of autoimmune > etiology and immune therapy for autism.> > As a neuroimmunologist, I have been interested in the immunology of the > nervous system, i.e., the immune basis and immune therapy for brain > diseases and mental illnesses. I have studied autism as an autoimmune > disorder for over fifteen years. As a result, 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. I recently postulated a > "Neuroautoimmunity Model of Autism" which I discussed at two recent > conferences: first, the Biomedical Treatments for Autism and PDD > Conference held in Orlando, Florida (May, 1999); and second, the > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in Bethesda, > land (June, 1999). Briefly, I hypothesized that an autoimmune > reaction to brain structures, in particular the myelin sheath, plays a > critical role in causing the neurological impairments of patients with > autism. I 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.> > I believe that autism can be treated successfully using some of the > therapies proven effective in treating other autoimmune diseases. I am > exploring specifically the role of autoimmune factors, (e.g., viruses, > autoantibodies, T cells, and cytokines) because they serve as the prime > targets of therapy with immune-modulating agents. I emphasize the need > to focus on immunotherapies, and I urge doctors toexamine autoimmunity > as a novel target on which to focus in treating autistic patients. > There is enormous potential for restoring brain function in autistic > children and adults through immunology.> > Autoimmune Etiology in Autism> > A disease is commonly 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. While some > of the key features are listed below, I will focus more on the current > research relating to three topics: viral studies; autoimmune testing; > and autoimmune therapy. 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, extended haplotypes, etc.> > 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 respond well to immune therapies.> > Viral Studies in Autism> > Viruses have been linked to autism, but this relationship is far from > fully explored. 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 was 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 never been investigated, I think this > is due to a defect in T lymphocytes-these agents of immune response are > not functioning properly in these children. In an unpublished pilot > study, I found that the RV-induced lymphocyte proliferation response in > autistic children was only one-fourth of the response in normal > children, which clearly suggests a defect of T cell-mediated immunity > (a defense mechanism that helps fight virus infections).> > 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. A few years > ago I and coworkers conducted a study of IgG antibodies to CMV; we > found no statistical difference between autistic children and normal > children (V. Singh, D. Schubert and R. Warren, 1992; unpublished data). > Simply put, this means that CMV is probably not related to autism.> > More recently, I conducted a study of measles virus (MV) and human > herpesvirus-6 (HHV-6) in autism. This was done by two types of > laboratory analysis: (a) virus antibody levels of MV and HHV-6; and ( > brain autoantibody titers in the same samples as those assayed for > virus antibodies. 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 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 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.> > Testing for Autoimmunity in Autism> > Recent advances have clearly shown that autoimmunity plays a key role > in the pathogenesis of autism. Since the brain is the affected organ in > autism, the autoimmune response will be directed against this organ. > This response is commonly identified by certain autoimmune factors > which I have identified in autistic children. The list includes> brain-specific autoantibodies, viral antibodies, cytokine profile or> immune activation markers, as well as antinuclear antibodies. > Collectively, they are essential for identifying a brain-specific > autoimmune response, which can afterward be treated with immune > therapy. By performing blood tests we can determine if a patient shows > autoimmunity to brain tissues, if he or she is a candidate for> experimental immune therapy, and if the response to therapy is> effective. Therefore, this type of immune evaluation is very important> in helping children with autism.> > Brain autoantibodies: this test detects antibodies to two brain > proteins, namely 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. It is, however, recommended that the two > markers be tested simultaneously.> > Cytokine profile: 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: this test 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: this test assays for antinuclear antibodies> (ANA). They are non-specific antibodies but are often present in> patients with autoimmune diseases. Approximately one-third of autistic> children tested have positive titers of ANA (V. Singh, 1992;> unpublished data).> > Immunotherapy in Autism> > The aforementioned laboratory findings clearly point to an autoimmune > pathogenic mechanism in autism. The idea that autism is an autoimmune > disorder is further strengthened by the fact that autistic patients > respond well to treatment with immune modulating drugs. Immune > interventions can produce immune modulation-a state of suppression or > stimulation. Depending on the nature of the immune abnormality, 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. Immune therapy should always be done in consultation > with physicians. The following immune interventions can be used:> > Steroid therapy: steroids such as Prednisone and/or ACTH> (adrenocorticotropin hormone) are commonly used as anti-inflammatory> and/or immunosuppressive drugs for treating patients with autoimmune> diseases, inflammatory diseases, etc. In autism, however, there is only> one study that showed improvement of autistic-like symptoms in children> when they were treated with an ACTH analogue. This result indicated> that steroids are potentially useful in alleviating clinical symptoms> of autism. Steroids are the first course of treatment for patients with> autoimmune diseases and infantile spasm; however, their efficacy has> not been evaluated in autism.> > Intraveneous immunoglobulin (IVIG): this type of treatment has been> used to treat children with autism. Open-label trials of both low-dose> and high-dose IVIG have shown that most but not all autistic children> respond favorably to this treatment. My collaborators and I recently> found that the high-dose IVIG was better than the low-dose IVIG (J.> Bradstreet, V. Singh and J. El-Dahr, paper presented at the> International Symposium on Autism, Netherlands, December 28-30, 1999).> Clinically, children so treated have shown improvements in language,> communication, social interaction and attention span. In a double-blind> study, (V. Singh, 1997; unpublished data) the IVIG treatment was found> to decrease brain autoantibody titers in five patients (they were> positive pre-therapy but became virtually negative post-therapy) who> also showed clinical improvement of autistic characteristics. In spite> of the success of IVIG, this treatment is not for everyone. Before this> treatment is administered, a proper immune evaluation is highly> recommended to assess the nature of the immune problem.> > Oral tolerance with autoantigens: this treatment is a means of inducing > immune suppression by feeding patients autoantigen. I have shown that > the candidate autoantigen in autism appeared to be a myelin basic > protein (MBP); this suggested that the MBP-containing myelin products > can be used to treat autistic patients. Indeed, one such product known > as Sphingolin has been used with success. Recently, the parents, school> psychologists, and other professionals have anecdotally reported > tremendous improvements of autistic symptoms in their children. These > reports are undoubtedly quite encouraging and promising, but a > well-designed clinical trial is warranted.> > Plasmapheresis: although it is not commonly recommended, this procedure> is used for treating patients with infections, autoimmune diseases,> immune complex diseases, etc. Because this method removes harmful> substances (e.g., autoantibodies) from the blood, it is considered a> viable immune therapy. The method has been used to treat certain brain> disorders, for example Rasmussen's encephalitis (RE) and> obsessive-compulsive disorder (OCD), in which autoimmunity has been> implicated as a basis of the disorder. Plasmapheresis produced positive> responses in patients with these disorders, and the responses were much> better with plasmapheresis when compared to the IVIG treatment. In each> case, the benefit to the patient was associated with the lowering of> the anti-neuronal antibody titers. Since autistic patients also have> positive titers of brain autoantibodies, they should also respond to> plasmapheresis. Although this treatment has long been suggested for use> in autism (V. Singh, 1997), plasmapheresis has thus far not been tried> in patients with this disorder.> > Conclusion> > The evidence is rapidly accumulating to suggest that autism is an > autoimmune disorder. The autoimmune response is most likely directed > against the brain myelin, perhaps secondary to a viral infection. > Measles virus is a candidate but other possibilities remain to be > explored. More importantly, the patients respond to treatment with > immune therapies. Therefore, I conclude that autoimmunity offersstrong > prospects for drug discovery and therapy for autism. Naturally, it > deserves prompt attention from all those who want to help people with > autism.> > Selected Reading> > Singh, V. K., "Plasma Increase of Interleukin-12 and Interferon-gamma: > Pathological Significance in Autism" (Journal of Neuroimmunology, vol. > 66, pp. 143-145 [1996]).> > Singh, V. K., "Immunotherapy for Brain Diseases and Mental Illnesses,"> (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).> > Singh, V. K., "Serological Association of Measles Virus and Human > Herpesvirus-6 With Brain Autoantibodies in Autism" (Clinical Immunology > and Immunopathology, vol. 89, pp. 105-108 [1998]).> > Singh, V. K., "Autoimmunity and Neurologic Disorders" (Latitudes, vol.> 4, pp. 5-11 [1999]).> > Dr. Singh received his doctorate from the University of British > Columbia, Vancouver, Canada. His post-doctoral fellowship was completed > in neurochemistry and neuroimmunology. Spanning over twenty years' > experience in neurobiology and immunology research, Dr. Singh studied > brain diseases, particularly infantile autism and Alzheimer's disease. > Having authored over a hundred scientific publications, he is both a > pioneer and an international authority on autoimmunity in autism. Dr. > Singh is a member of the American Association for the Advancement of > Sciences, the American Association of Immunologists, and the New York > Academy of Sciences. He is listed in American Men and Women in Science > (United States, R. R. Bowker, publisher) and The International Who's > Who of Intellectuals (Cambridge, England, International Biographical > Centre).> > For further information, please contact Dr. Vijendra Singh, Ph.D., at > the Biotechnology Center, Department of Biology, Utah State University, > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail: > singhvk@...].> > Reprinted from AAPN, The Autism Autoimmunity Project Newsletter, vol. 1,> number 2, December 1999.> > > > Links> > "Autoimmunity and Neurological Disorders," interview with V. K. Singh in> Latitudes, newsletter of the Association for> Comprehensive NeuroTherapy, http://www.latitudes.org/index.html, vol. 4,> no. 2, Spring 1999, by Sheila> : http://lib.tcu.edu/www/staff/lruede/latitudes> > "V. K. Singh: Selected Research on Autism," http://www.gti.net/truegrit/> : Findings in Immunology> > "Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease,"> (http://lib.tcu.edu/www/staff/lruede/alzheimers)> > > > > > __________________________________________________> > Correo Yahoo!> > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!> > Regístrate ya - http://correo.espanol.yahoo.com/> >>

[Guest guest]

So, say you were lucky enough to be able to get these tests done,

what do you do with the info, are there doctors in the UK ready to

provide " treatment " ?

My son's cousins have MS x 2 and Muscular Dystrophy x 2 and

rheumatoid arthritis and other auto immune diseases.

Anyone know if research is being done in this regard over here and

who to contact?

I am very interested in the Sphingolin. Any more info about this

much appreciated.

thanks

>

> ... I find it very odd that his findings and suggestions have not

been

> explored by DAN! and others to greater extent!

>

> I have saved the text below a while ago, someone brought up

discussion

> on one of the treatments..

>

> here is a bit more on his work:

> http://www.latitudes.org/articles/singh_neuro_ts.html

>

>

> 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

>

> Autism is an early-onset biological disorder that causes severe

> deficits of higher mental functions, as well as behavioral

> manifestations. There is no single, clear-cut cause and no

complete

> cure for autism. Causally speaking, immune factors, neuro-chemical

> factors, genetic susceptibility factors and environmental factors

(such

> as microbial infections and chemical toxicity) have been

implicated. I

> view autism as a very complex, multifactorial disorder. In this

> article, I will attempt to describe succinctly the role of

autoimmune

> etiology and immune therapy for autism.

>

> As a neuroimmunologist, I have been interested in the immunology

of the

> nervous system, i.e., the immune basis and immune therapy for

brain

> diseases and mental illnesses. I have studied autism as an

autoimmune

> disorder for over fifteen years. As a result, 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. I recently postulated a

> " Neuroautoimmunity Model of Autism " which I discussed at two

recent

> conferences: first, the Biomedical Treatments for Autism and PDD

> Conference held in Orlando, Florida (May, 1999); and second, the

> Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

Bethesda,

> land (June, 1999). Briefly, I hypothesized that an autoimmune

> reaction to brain structures, in particular the myelin sheath,

plays a

> critical role in causing the neurological impairments of patients

with

> autism. I 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.

>

> I believe that autism can be treated successfully using some of

the

> therapies proven effective in treating other autoimmune diseases.

I am

> exploring specifically the role of autoimmune factors, (e.g.,

viruses,

> autoantibodies, T cells, and cytokines) because they serve as the

prime

> targets of therapy with immune-modulating agents. I emphasize the

need

> to focus on immunotherapies, and I urge doctors toexamine

autoimmunity

> as a novel target on which to focus in treating autistic patients.

> There is enormous potential for restoring brain function in

autistic

> children and adults through immunology.

>

> Autoimmune Etiology in Autism

>

> A disease is commonly 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. While

some

> of the key features are listed below, I will focus more on the

current

> research relating to three topics: viral studies; autoimmune

testing;

> and autoimmune therapy. 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, extended haplotypes, etc.

>

> 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 respond well to immune therapies.

>

> Viral Studies in Autism

>

> Viruses have been linked to autism, but this relationship is far

from

> fully explored. 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 was 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 never been investigated, I think

this

> is due to a defect in T lymphocytes-these agents of immune

response are

> not functioning properly in these children. In an unpublished

pilot

> study, I found that the RV-induced lymphocyte proliferation

response in

> autistic children was only one-fourth of the response in normal

> children, which clearly suggests a defect of T cell-mediated

immunity

> (a defense mechanism that helps fight virus infections).

>

> 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. A few

years

> ago I and coworkers conducted a study of IgG antibodies to CMV; we

> found no statistical difference between autistic children and

normal

> children (V. Singh, D. Schubert and R. Warren, 1992; unpublished

data).

> Simply put, this means that CMV is probably not related to autism.

>

> More recently, I conducted a study of measles virus (MV) and human

> herpesvirus-6 (HHV-6) in autism. This was done by two types of

> laboratory analysis: (a) virus antibody levels of MV and HHV-6;

and (

> brain autoantibody titers in the same samples as those assayed for

> virus antibodies. 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

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 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.

>

> Testing for Autoimmunity in Autism

>

> Recent advances have clearly shown that autoimmunity plays a key

role

> in the pathogenesis of autism. Since the brain is the affected

organ in

> autism, the autoimmune response will be directed against this

organ.

> This response is commonly identified by certain autoimmune factors

> which I have identified in autistic children. The list includes

> brain-specific autoantibodies, viral antibodies, cytokine profile

or

> immune activation markers, as well as antinuclear antibodies.

> Collectively, they are essential for identifying a brain-specific

> autoimmune response, which can afterward be treated with immune

> therapy. By performing blood tests we can determine if a patient

shows

> autoimmunity to brain tissues, if he or she is a candidate for

> experimental immune therapy, and if the response to therapy is

> effective. Therefore, this type of immune evaluation is very

important

> in helping children with autism.

>

> Brain autoantibodies: this test detects antibodies to two brain

> proteins, namely 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. It is, however, recommended that the two

> markers be tested simultaneously.

>

> Cytokine profile: 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: this test 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: this test assays for antinuclear

antibodies

> (ANA). They are non-specific antibodies but are often present in

> patients with autoimmune diseases. Approximately one-third of

autistic

> children tested have positive titers of ANA (V. Singh, 1992;

> unpublished data).

>

> Immunotherapy in Autism

>

> The aforementioned laboratory findings clearly point to an

autoimmune

> pathogenic mechanism in autism. The idea that autism is an

autoimmune

> disorder is further strengthened by the fact that autistic

patients

> respond well to treatment with immune modulating drugs. Immune

> interventions can produce immune modulation-a state of suppression

or

> stimulation. Depending on the nature of the immune abnormality,

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. Immune therapy should always be done in

consultation

> with physicians. The following immune interventions can be used:

>

> Steroid therapy: steroids such as Prednisone and/or ACTH

> (adrenocorticotropin hormone) are commonly used as anti-

inflammatory

> and/or immunosuppressive drugs for treating patients with

autoimmune

> diseases, inflammatory diseases, etc. In autism, however, there

is only

> one study that showed improvement of autistic-like symptoms in

children

> when they were treated with an ACTH analogue. This result

indicated

> that steroids are potentially useful in alleviating clinical

symptoms

> of autism. Steroids are the first course of treatment for

patients with

> autoimmune diseases and infantile spasm; however, their efficacy

has

> not been evaluated in autism.

>

> Intraveneous immunoglobulin (IVIG): this type of treatment has

been

> used to treat children with autism. Open-label trials of both low-

dose

> and high-dose IVIG have shown that most but not all autistic

children

> respond favorably to this treatment. My collaborators and I

recently

> found that the high-dose IVIG was better than the low-dose IVIG

(J.

> Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> International Symposium on Autism, Netherlands, December 28-30,

1999).

> Clinically, children so treated have shown improvements in

language,

> communication, social interaction and attention span. In a double-

blind

> study, (V. Singh, 1997; unpublished data) the IVIG treatment was

found

> to decrease brain autoantibody titers in five patients (they were

> positive pre-therapy but became virtually negative post-therapy)

who

> also showed clinical improvement of autistic characteristics. In

spite

> of the success of IVIG, this treatment is not for everyone.

Before this

> treatment is administered, a proper immune evaluation is highly

> recommended to assess the nature of the immune problem.

>

> Oral tolerance with autoantigens: this treatment is a means of

inducing

> immune suppression by feeding patients autoantigen. I have shown

that

> the candidate autoantigen in autism appeared to be a myelin basic

> protein (MBP); this suggested that the MBP-containing myelin

products

> can be used to treat autistic patients. Indeed, one such product

known

> as Sphingolin has been used with success. Recently, the parents,

school

> psychologists, and other professionals have anecdotally reported

> tremendous improvements of autistic symptoms in their children.

These

> reports are undoubtedly quite encouraging and promising, but a

> well-designed clinical trial is warranted.

>

> Plasmapheresis: although it is not commonly recommended, this

procedure

> is used for treating patients with infections, autoimmune

diseases,

> immune complex diseases, etc. Because this method removes harmful

> substances (e.g., autoantibodies) from the blood, it is

considered a

> viable immune therapy. The method has been used to treat certain

brain

> disorders, for example Rasmussen's encephalitis (RE) and

> obsessive-compulsive disorder (OCD), in which autoimmunity has

been

> implicated as a basis of the disorder. Plasmapheresis produced

positive

> responses in patients with these disorders, and the responses

were much

> better with plasmapheresis when compared to the IVIG treatment.

In each

> case, the benefit to the patient was associated with the lowering

of

> the anti-neuronal antibody titers. Since autistic patients also

have

> positive titers of brain autoantibodies, they should also respond

to

> plasmapheresis. Although this treatment has long been suggested

for use

> in autism (V. Singh, 1997), plasmapheresis has thus far not been

tried

> in patients with this disorder.

>

> Conclusion

>

> The evidence is rapidly accumulating to suggest that autism is an

> autoimmune disorder. The autoimmune response is most likely

directed

> against the brain myelin, perhaps secondary to a viral infection.

> Measles virus is a candidate but other possibilities remain to be

> explored. More importantly, the patients respond to treatment with

> immune therapies. Therefore, I conclude that autoimmunity

offersstrong

> prospects for drug discovery and therapy for autism. Naturally, it

> deserves prompt attention from all those who want to help people

with

> autism.

>

> Selected Reading

>

> Singh, V. K., " Plasma Increase of Interleukin-12 and Interferon-

gamma:

> Pathological Significance in Autism " (Journal of Neuroimmunology,

vol.

> 66, pp. 143-145 [1996]).

>

> Singh, V. K., " Immunotherapy for Brain Diseases and Mental

Illnesses, "

> (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

>

> Singh, V. K., " Serological Association of Measles Virus and Human

> Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

Immunology

> and Immunopathology, vol. 89, pp. 105-108 [1998]).

>

> Singh, V. K., " Autoimmunity and Neurologic Disorders " (Latitudes,

vol.

> 4, pp. 5-11 [1999]).

>

> Dr. Singh received his doctorate from the University of British

> Columbia, Vancouver, Canada. His post-doctoral fellowship was

completed

> in neurochemistry and neuroimmunology. Spanning over twenty years'

> experience in neurobiology and immunology research, Dr. Singh

studied

> brain diseases, particularly infantile autism and Alzheimer's

disease.

> Having authored over a hundred scientific publications, he is both

a

> pioneer and an international authority on autoimmunity in autism.

Dr.

> Singh is a member of the American Association for the Advancement

of

> Sciences, the American Association of Immunologists, and the New

York

> Academy of Sciences. He is listed in American Men and Women in

Science

> (United States, R. R. Bowker, publisher) and The International

Who's

> Who of Intellectuals (Cambridge, England, International

Biographical

> Centre).

>

> For further information, please contact Dr. Vijendra Singh, Ph.D.,

at

> the Biotechnology Center, Department of Biology, Utah State

University,

> 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> singhvk@...].

>

> Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,

vol. 1,

> number 2, December 1999.

>

>

>

> Links

>

> " Autoimmunity and Neurological Disorders, " interview with V. K.

Singh in

> Latitudes, newsletter of the Association for

> Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,

vol. 4,

> no. 2, Spring 1999, by Sheila

> : http://lib.tcu.edu/www/staff/lruede/latitudes

>

> " V. K. Singh: Selected Research on Autism, "

http://www.gti.net/truegrit/

> : Findings in Immunology

>

> " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease, "

> (http://lib.tcu.edu/www/staff/lruede/alzheimers)

>

>

>

>

> > __________________________________________________

> > Correo Yahoo!

> > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > Regístrate ya - http://correo.espanol.yahoo.com/

> >

>

[Guest guest]

The nearest people I know of who view and treat autism as primarily

auto/immune disorders are in New York...

have a look at this, as Vit D is recommended for all of these (makes a

lot of sense in the light of recent findings of it regulating

inflammation and stopping autoimmunity by inhibiting excessive

production of cytokines )

http://www.vitamindcouncil.com/

fwiw they do not recommend Cod liver oil as a source of vit D , but the

reasons they give do not hold water imo, will write to them for

clarification or correction...

you (and cousins) also want to look at anything else that increases

Il-10 - reg cytokine, and lowers the others, esp Il-2/12/23 as these

are thought to be involved in developing autoimmunity...

LDN is helpful for MS...

natasa

> >

> > ... I find it very odd that his findings and suggestions have not

> been

> > explored by DAN! and others to greater extent!

> >

> > I have saved the text below a while ago, someone brought up

> discussion

> > on one of the treatments..

> >

> > here is a bit more on his work:

> > http://www.latitudes.org/articles/singh_neuro_ts.html

> >

> >

> > 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

> >

> > Autism is an early-onset biological disorder that causes severe

> > deficits of higher mental functions, as well as behavioral

> > manifestations. There is no single, clear-cut cause and no

> complete

> > cure for autism. Causally speaking, immune factors, neuro-chemical

> > factors, genetic susceptibility factors and environmental factors

> (such

> > as microbial infections and chemical toxicity) have been

> implicated. I

> > view autism as a very complex, multifactorial disorder. In this

> > article, I will attempt to describe succinctly the role of

> autoimmune

> > etiology and immune therapy for autism.

> >

> > As a neuroimmunologist, I have been interested in the immunology

> of the

> > nervous system, i.e., the immune basis and immune therapy for

> brain

> > diseases and mental illnesses. I have studied autism as an

> autoimmune

> > disorder for over fifteen years. As a result, 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. I recently postulated a

> > " Neuroautoimmunity Model of Autism " which I discussed at two

> recent

> > conferences: first, the Biomedical Treatments for Autism and PDD

> > Conference held in Orlando, Florida (May, 1999); and second, the

> > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

> Bethesda,

> > land (June, 1999). Briefly, I hypothesized that an autoimmune

> > reaction to brain structures, in particular the myelin sheath,

> plays a

> > critical role in causing the neurological impairments of patients

> with

> > autism. I 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.

> >

> > I believe that autism can be treated successfully using some of

> the

> > therapies proven effective in treating other autoimmune diseases.

> I am

> > exploring specifically the role of autoimmune factors, (e.g.,

> viruses,

> > autoantibodies, T cells, and cytokines) because they serve as the

> prime

> > targets of therapy with immune-modulating agents. I emphasize the

> need

> > to focus on immunotherapies, and I urge doctors toexamine

> autoimmunity

> > as a novel target on which to focus in treating autistic patients.

> > There is enormous potential for restoring brain function in

> autistic

> > children and adults through immunology.

> >

> > Autoimmune Etiology in Autism

> >

> > A disease is commonly 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. While

> some

> > of the key features are listed below, I will focus more on the

> current

> > research relating to three topics: viral studies; autoimmune

> testing;

> > and autoimmune therapy. 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, extended haplotypes, etc.

> >

> > 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 respond well to immune therapies.

> >

> > Viral Studies in Autism

> >

> > Viruses have been linked to autism, but this relationship is far

> from

> > fully explored. 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 was 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 never been investigated, I think

> this

> > is due to a defect in T lymphocytes-these agents of immune

> response are

> > not functioning properly in these children. In an unpublished

> pilot

> > study, I found that the RV-induced lymphocyte proliferation

> response in

> > autistic children was only one-fourth of the response in normal

> > children, which clearly suggests a defect of T cell-mediated

> immunity

> > (a defense mechanism that helps fight virus infections).

> >

> > 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. A few

> years

> > ago I and coworkers conducted a study of IgG antibodies to CMV; we

> > found no statistical difference between autistic children and

> normal

> > children (V. Singh, D. Schubert and R. Warren, 1992; unpublished

> data).

> > Simply put, this means that CMV is probably not related to autism.

> >

> > More recently, I conducted a study of measles virus (MV) and human

> > herpesvirus-6 (HHV-6) in autism. This was done by two types of

> > laboratory analysis: (a) virus antibody levels of MV and HHV-6;

> and (

> > brain autoantibody titers in the same samples as those assayed for

> > virus antibodies. 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

> 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 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.

> >

> > Testing for Autoimmunity in Autism

> >

> > Recent advances have clearly shown that autoimmunity plays a key

> role

> > in the pathogenesis of autism. Since the brain is the affected

> organ in

> > autism, the autoimmune response will be directed against this

> organ.

> > This response is commonly identified by certain autoimmune factors

> > which I have identified in autistic children. The list includes

> > brain-specific autoantibodies, viral antibodies, cytokine profile

> or

> > immune activation markers, as well as antinuclear antibodies.

> > Collectively, they are essential for identifying a brain-specific

> > autoimmune response, which can afterward be treated with immune

> > therapy. By performing blood tests we can determine if a patient

> shows

> > autoimmunity to brain tissues, if he or she is a candidate for

> > experimental immune therapy, and if the response to therapy is

> > effective. Therefore, this type of immune evaluation is very

> important

> > in helping children with autism.

> >

> > Brain autoantibodies: this test detects antibodies to two brain

> > proteins, namely 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. It is, however, recommended that the two

> > markers be tested simultaneously.

> >

> > Cytokine profile: 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: this test 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: this test assays for antinuclear

> antibodies

> > (ANA). They are non-specific antibodies but are often present in

> > patients with autoimmune diseases. Approximately one-third of

> autistic

> > children tested have positive titers of ANA (V. Singh, 1992;

> > unpublished data).

> >

> > Immunotherapy in Autism

> >

> > The aforementioned laboratory findings clearly point to an

> autoimmune

> > pathogenic mechanism in autism. The idea that autism is an

> autoimmune

> > disorder is further strengthened by the fact that autistic

> patients

> > respond well to treatment with immune modulating drugs. Immune

> > interventions can produce immune modulation-a state of suppression

> or

> > stimulation. Depending on the nature of the immune abnormality,

> 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. Immune therapy should always be done in

> consultation

> > with physicians. The following immune interventions can be used:

> >

> > Steroid therapy: steroids such as Prednisone and/or ACTH

> > (adrenocorticotropin hormone) are commonly used as anti-

> inflammatory

> > and/or immunosuppressive drugs for treating patients with

> autoimmune

> > diseases, inflammatory diseases, etc. In autism, however, there

> is only

> > one study that showed improvement of autistic-like symptoms in

> children

> > when they were treated with an ACTH analogue. This result

> indicated

> > that steroids are potentially useful in alleviating clinical

> symptoms

> > of autism. Steroids are the first course of treatment for

> patients with

> > autoimmune diseases and infantile spasm; however, their efficacy

> has

> > not been evaluated in autism.

> >

> > Intraveneous immunoglobulin (IVIG): this type of treatment has

> been

> > used to treat children with autism. Open-label trials of both low-

> dose

> > and high-dose IVIG have shown that most but not all autistic

> children

> > respond favorably to this treatment. My collaborators and I

> recently

> > found that the high-dose IVIG was better than the low-dose IVIG

> (J.

> > Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> > International Symposium on Autism, Netherlands, December 28-30,

> 1999).

> > Clinically, children so treated have shown improvements in

> language,

> > communication, social interaction and attention span. In a double-

> blind

> > study, (V. Singh, 1997; unpublished data) the IVIG treatment was

> found

> > to decrease brain autoantibody titers in five patients (they were

> > positive pre-therapy but became virtually negative post-therapy)

> who

> > also showed clinical improvement of autistic characteristics. In

> spite

> > of the success of IVIG, this treatment is not for everyone.

> Before this

> > treatment is administered, a proper immune evaluation is highly

> > recommended to assess the nature of the immune problem.

> >

> > Oral tolerance with autoantigens: this treatment is a means of

> inducing

> > immune suppression by feeding patients autoantigen. I have shown

> that

> > the candidate autoantigen in autism appeared to be a myelin basic

> > protein (MBP); this suggested that the MBP-containing myelin

> products

> > can be used to treat autistic patients. Indeed, one such product

> known

> > as Sphingolin has been used with success. Recently, the parents,

> school

> > psychologists, and other professionals have anecdotally reported

> > tremendous improvements of autistic symptoms in their children.

> These

> > reports are undoubtedly quite encouraging and promising, but a

> > well-designed clinical trial is warranted.

> >

> > Plasmapheresis: although it is not commonly recommended, this

> procedure

> > is used for treating patients with infections, autoimmune

> diseases,

> > immune complex diseases, etc. Because this method removes harmful

> > substances (e.g., autoantibodies) from the blood, it is

> considered a

> > viable immune therapy. The method has been used to treat certain

> brain

> > disorders, for example Rasmussen's encephalitis (RE) and

> > obsessive-compulsive disorder (OCD), in which autoimmunity has

> been

> > implicated as a basis of the disorder. Plasmapheresis produced

> positive

> > responses in patients with these disorders, and the responses

> were much

> > better with plasmapheresis when compared to the IVIG treatment.

> In each

> > case, the benefit to the patient was associated with the lowering

> of

> > the anti-neuronal antibody titers. Since autistic patients also

> have

> > positive titers of brain autoantibodies, they should also respond

> to

> > plasmapheresis. Although this treatment has long been suggested

> for use

> > in autism (V. Singh, 1997), plasmapheresis has thus far not been

> tried

> > in patients with this disorder.

> >

> > Conclusion

> >

> > The evidence is rapidly accumulating to suggest that autism is an

> > autoimmune disorder. The autoimmune response is most likely

> directed

> > against the brain myelin, perhaps secondary to a viral infection.

> > Measles virus is a candidate but other possibilities remain to be

> > explored. More importantly, the patients respond to treatment with

> > immune therapies. Therefore, I conclude that autoimmunity

> offersstrong

> > prospects for drug discovery and therapy for autism. Naturally, it

> > deserves prompt attention from all those who want to help people

> with

> > autism.

> >

> > Selected Reading

> >

> > Singh, V. K., " Plasma Increase of Interleukin-12 and Interferon-

> gamma:

> > Pathological Significance in Autism " (Journal of Neuroimmunology,

> vol.

> > 66, pp. 143-145 [1996]).

> >

> > Singh, V. K., " Immunotherapy for Brain Diseases and Mental

> Illnesses, "

> > (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

> >

> > Singh, V. K., " Serological Association of Measles Virus and Human

> > Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

> Immunology

> > and Immunopathology, vol. 89, pp. 105-108 [1998]).

> >

> > Singh, V. K., " Autoimmunity and Neurologic Disorders " (Latitudes,

> vol.

> > 4, pp. 5-11 [1999]).

> >

> > Dr. Singh received his doctorate from the University of British

> > Columbia, Vancouver, Canada. His post-doctoral fellowship was

> completed

> > in neurochemistry and neuroimmunology. Spanning over twenty years'

> > experience in neurobiology and immunology research, Dr. Singh

> studied

> > brain diseases, particularly infantile autism and Alzheimer's

> disease.

> > Having authored over a hundred scientific publications, he is both

> a

> > pioneer and an international authority on autoimmunity in autism.

> Dr.

> > Singh is a member of the American Association for the Advancement

> of

> > Sciences, the American Association of Immunologists, and the New

> York

> > Academy of Sciences. He is listed in American Men and Women in

> Science

> > (United States, R. R. Bowker, publisher) and The International

> Who's

> > Who of Intellectuals (Cambridge, England, International

> Biographical

> > Centre).

> >

> > For further information, please contact Dr. Vijendra Singh, Ph.D.,

> at

> > the Biotechnology Center, Department of Biology, Utah State

> University,

> > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> > singhvk@].

> >

> > Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,

> vol. 1,

> > number 2, December 1999.

> >

> >

> >

> > Links

> >

> > " Autoimmunity and Neurological Disorders, " interview with V. K.

> Singh in

> > Latitudes, newsletter of the Association for

> > Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,

> vol. 4,

> > no. 2, Spring 1999, by Sheila

> > : http://lib.tcu.edu/www/staff/lruede/latitudes

> >

> > " V. K. Singh: Selected Research on Autism, "

> http://www.gti.net/truegrit/

> > : Findings in Immunology

> >

> > " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease, "

> > (http://lib.tcu.edu/www/staff/lruede/alzheimers)

> >

> >

> >

> >

> > > __________________________________________________

> > > Correo Yahoo!

> > > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > > Regístrate ya - http://correo.espanol.yahoo.com/

> > >

> >

>

[Guest guest]

On the contrary , this is anything BUT a single approach! Read a

bit on what this guy is actually saying as the opposite is actually the

case - his 'single' theory of ASD etiology (and recommended tests and

eventual treatment options) is the most complex I have read to date.

fwiw the fact that he skips some of the more common treatments is that

he may well be after the core problems, by the look of it.

it could well be that it fell weyside as it is very complex and not many

DAN!s out there who have the necessary knowledge and expertise, if

anyone.

natasa

> >

> > ... I find it very odd that his findings and suggestions have not

> been

> > explored by DAN! and others to greater extent!

> >

> > I have saved the text below a while ago, someone brought up

> discussion

> > on one of the treatments..

> >

> > here is a bit more on his work:

> > http://www.latitudes.org/articles/singh_neuro_ts.html

> >

> >

> > 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

> >

> > Autism is an early-onset biological disorder that causes severe

> > deficits of higher mental functions, as well as behavioral

> > manifestations. There is no single, clear-cut cause and no

> complete

> > cure for autism. Causally speaking, immune factors, neuro-chemical

> > factors, genetic susceptibility factors and environmental factors

> (such

> > as microbial infections and chemical toxicity) have been

> implicated. I

> > view autism as a very complex, multifactorial disorder. In this

> > article, I will attempt to describe succinctly the role of

> autoimmune

> > etiology and immune therapy for autism.

> >

> > As a neuroimmunologist, I have been interested in the immunology

> of the

> > nervous system, i.e., the immune basis and immune therapy for

> brain

> > diseases and mental illnesses. I have studied autism as an

> autoimmune

> > disorder for over fifteen years. As a result, 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. I recently postulated a

> > " Neuroautoimmunity Model of Autism " which I discussed at two

> recent

> > conferences: first, the Biomedical Treatments for Autism and PDD

> > Conference held in Orlando, Florida (May, 1999); and second, the

> > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

> Bethesda,

> > land (June, 1999). Briefly, I hypothesized that an autoimmune

> > reaction to brain structures, in particular the myelin sheath,

> plays a

> > critical role in causing the neurological impairments of patients

> with

> > autism. I 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.

> >

> > I believe that autism can be treated successfully using some of

> the

> > therapies proven effective in treating other autoimmune diseases.

> I am

> > exploring specifically the role of autoimmune factors, (e.g.,

> viruses,

> > autoantibodies, T cells, and cytokines) because they serve as the

> prime

> > targets of therapy with immune-modulating agents. I emphasize the

> need

> > to focus on immunotherapies, and I urge doctors toexamine

> autoimmunity

> > as a novel target on which to focus in treating autistic patients.

> > There is enormous potential for restoring brain function in

> autistic

> > children and adults through immunology.

> >

> > Autoimmune Etiology in Autism

> >

> > A disease is commonly 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. While

> some

> > of the key features are listed below, I will focus more on the

> current

> > research relating to three topics: viral studies; autoimmune

> testing;

> > and autoimmune therapy. 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, extended haplotypes, etc.

> >

> > 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 respond well to immune therapies.

> >

> > Viral Studies in Autism

> >

> > Viruses have been linked to autism, but this relationship is far

> from

> > fully explored. 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 was 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 never been investigated, I think

> this

> > is due to a defect in T lymphocytes-these agents of immune

> response are

> > not functioning properly in these children. In an unpublished

> pilot

> > study, I found that the RV-induced lymphocyte proliferation

> response in

> > autistic children was only one-fourth of the response in normal

> > children, which clearly suggests a defect of T cell-mediated

> immunity

> > (a defense mechanism that helps fight virus infections).

> >

> > 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. A few

> years

> > ago I and coworkers conducted a study of IgG antibodies to CMV; we

> > found no statistical difference between autistic children and

> normal

> > children (V. Singh, D. Schubert and R. Warren, 1992; unpublished

> data).

> > Simply put, this means that CMV is probably not related to autism.

> >

> > More recently, I conducted a study of measles virus (MV) and human

> > herpesvirus-6 (HHV-6) in autism. This was done by two types of

> > laboratory analysis: (a) virus antibody levels of MV and HHV-6;

> and (

> > brain autoantibody titers in the same samples as those assayed for

> > virus antibodies. 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

> 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 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.

> >

> > Testing for Autoimmunity in Autism

> >

> > Recent advances have clearly shown that autoimmunity plays a key

> role

> > in the pathogenesis of autism. Since the brain is the affected

> organ in

> > autism, the autoimmune response will be directed against this

> organ.

> > This response is commonly identified by certain autoimmune factors

> > which I have identified in autistic children. The list includes

> > brain-specific autoantibodies, viral antibodies, cytokine profile

> or

> > immune activation markers, as well as antinuclear antibodies.

> > Collectively, they are essential for identifying a brain-specific

> > autoimmune response, which can afterward be treated with immune

> > therapy. By performing blood tests we can determine if a patient

> shows

> > autoimmunity to brain tissues, if he or she is a candidate for

> > experimental immune therapy, and if the response to therapy is

> > effective. Therefore, this type of immune evaluation is very

> important

> > in helping children with autism.

> >

> > Brain autoantibodies: this test detects antibodies to two brain

> > proteins, namely 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. It is, however, recommended that the two

> > markers be tested simultaneously.

> >

> > Cytokine profile: 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: this test 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: this test assays for antinuclear

> antibodies

> > (ANA). They are non-specific antibodies but are often present in

> > patients with autoimmune diseases. Approximately one-third of

> autistic

> > children tested have positive titers of ANA (V. Singh, 1992;

> > unpublished data).

> >

> > Immunotherapy in Autism

> >

> > The aforementioned laboratory findings clearly point to an

> autoimmune

> > pathogenic mechanism in autism. The idea that autism is an

> autoimmune

> > disorder is further strengthened by the fact that autistic

> patients

> > respond well to treatment with immune modulating drugs. Immune

> > interventions can produce immune modulation-a state of suppression

> or

> > stimulation. Depending on the nature of the immune abnormality,

> 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. Immune therapy should always be done in

> consultation

> > with physicians. The following immune interventions can be used:

> >

> > Steroid therapy: steroids such as Prednisone and/or ACTH

> > (adrenocorticotropin hormone) are commonly used as anti-

> inflammatory

> > and/or immunosuppressive drugs for treating patients with

> autoimmune

> > diseases, inflammatory diseases, etc. In autism, however, there

> is only

> > one study that showed improvement of autistic-like symptoms in

> children

> > when they were treated with an ACTH analogue. This result

> indicated

> > that steroids are potentially useful in alleviating clinical

> symptoms

> > of autism. Steroids are the first course of treatment for

> patients with

> > autoimmune diseases and infantile spasm; however, their efficacy

> has

> > not been evaluated in autism.

> >

> > Intraveneous immunoglobulin (IVIG): this type of treatment has

> been

> > used to treat children with autism. Open-label trials of both low-

> dose

> > and high-dose IVIG have shown that most but not all autistic

> children

> > respond favorably to this treatment. My collaborators and I

> recently

> > found that the high-dose IVIG was better than the low-dose IVIG

> (J.

> > Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> > International Symposium on Autism, Netherlands, December 28-30,

> 1999).

> > Clinically, children so treated have shown improvements in

> language,

> > communication, social interaction and attention span. In a double-

> blind

> > study, (V. Singh, 1997; unpublished data) the IVIG treatment was

> found

> > to decrease brain autoantibody titers in five patients (they were

> > positive pre-therapy but became virtually negative post-therapy)

> who

> > also showed clinical improvement of autistic characteristics. In

> spite

> > of the success of IVIG, this treatment is not for everyone.

> Before this

> > treatment is administered, a proper immune evaluation is highly

> > recommended to assess the nature of the immune problem.

> >

> > Oral tolerance with autoantigens: this treatment is a means of

> inducing

> > immune suppression by feeding patients autoantigen. I have shown

> that

> > the candidate autoantigen in autism appeared to be a myelin basic

> > protein (MBP); this suggested that the MBP-containing myelin

> products

> > can be used to treat autistic patients. Indeed, one such product

> known

> > as Sphingolin has been used with success. Recently, the parents,

> school

> > psychologists, and other professionals have anecdotally reported

> > tremendous improvements of autistic symptoms in their children.

> These

> > reports are undoubtedly quite encouraging and promising, but a

> > well-designed clinical trial is warranted.

> >

> > Plasmapheresis: although it is not commonly recommended, this

> procedure

> > is used for treating patients with infections, autoimmune

> diseases,

> > immune complex diseases, etc. Because this method removes harmful

> > substances (e.g., autoantibodies) from the blood, it is

> considered a

> > viable immune therapy. The method has been used to treat certain

> brain

> > disorders, for example Rasmussen's encephalitis (RE) and

> > obsessive-compulsive disorder (OCD), in which autoimmunity has

> been

> > implicated as a basis of the disorder. Plasmapheresis produced

> positive

> > responses in patients with these disorders, and the responses

> were much

> > better with plasmapheresis when compared to the IVIG treatment.

> In each

> > case, the benefit to the patient was associated with the lowering

> of

> > the anti-neuronal antibody titers. Since autistic patients also

> have

> > positive titers of brain autoantibodies, they should also respond

> to

> > plasmapheresis. Although this treatment has long been suggested

> for use

> > in autism (V. Singh, 1997), plasmapheresis has thus far not been

> tried

> > in patients with this disorder.

> >

> > Conclusion

> >

> > The evidence is rapidly accumulating to suggest that autism is an

> > autoimmune disorder. The autoimmune response is most likely

> directed

> > against the brain myelin, perhaps secondary to a viral infection.

> > Measles virus is a candidate but other possibilities remain to be

> > explored. More importantly, the patients respond to treatment with

> > immune therapies. Therefore, I conclude that autoimmunity

> offersstrong

> > prospects for drug discovery and therapy for autism. Naturally, it

> > deserves prompt attention from all those who want to help people

> with

> > autism.

> >

> > Selected Reading

> >

> > Singh, V. K., " Plasma Increase of Interleukin-12 and Interferon-

> gamma:

> > Pathological Significance in Autism " (Journal of Neuroimmunology,

> vol.

> > 66, pp. 143-145 [1996]).

> >

> > Singh, V. K., " Immunotherapy for Brain Diseases and Mental

> Illnesses, "

> > (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

> >

> > Singh, V. K., " Serological Association of Measles Virus and Human

> > Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

> Immunology

> > and Immunopathology, vol. 89, pp. 105-108 [1998]).

> >

> > Singh, V. K., " Autoimmunity and Neurologic Disorders " (Latitudes,

> vol.

> > 4, pp. 5-11 [1999]).

> >

> > Dr. Singh received his doctorate from the University of British

> > Columbia, Vancouver, Canada. His post-doctoral fellowship was

> completed

> > in neurochemistry and neuroimmunology. Spanning over twenty years'

> > experience in neurobiology and immunology research, Dr. Singh

> studied

> > brain diseases, particularly infantile autism and Alzheimer's

> disease.

> > Having authored over a hundred scientific publications, he is both

> a

> > pioneer and an international authority on autoimmunity in autism.

> Dr.

> > Singh is a member of the American Association for the Advancement

> of

> > Sciences, the American Association of Immunologists, and the New

> York

> > Academy of Sciences. He is listed in American Men and Women in

> Science

> > (United States, R. R. Bowker, publisher) and The International

> Who's

> > Who of Intellectuals (Cambridge, England, International

> Biographical

> > Centre).

> >

> > For further information, please contact Dr. Vijendra Singh, Ph.D.,

> at

> > the Biotechnology Center, Department of Biology, Utah State

> University,

> > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> > singhvk@].

> >

> > Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,

> vol. 1,

> > number 2, December 1999.

> >

> >

> >

> > Links

> >

> > " Autoimmunity and Neurological Disorders, " interview with V. K.

> Singh in

> > Latitudes, newsletter of the Association for

> > Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,

> vol. 4,

> > no. 2, Spring 1999, by Sheila

> > : http://lib.tcu.edu/www/staff/lruede/latitudes

> >

> > " V. K. Singh: Selected Research on Autism, "

> http://www.gti.net/truegrit/

> > : Findings in Immunology

> >

> > " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease, "

> > (http://lib.tcu.edu/www/staff/lruede/alzheimers)

> >

> >

> >

> >

> > > __________________________________________________

> > > Correo Yahoo!

> > > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > > Regístrate ya - http://correo.espanol.yahoo.com/

> > >

> >

>

[Guest guest]

i AGREE Natasa, we used 2 years to get our boy's gut in order via

McCandless, etc. His gut is still not well, and more issues have

come up, bigger issues.

It really is up to each individual parent isnt it, to do the

research, the tests and often interpret them for our individual

children.

I learned a while back, no help is a coming, except from other

parents. Have yet to find a multidisciplinary doctor who is willing

or able to take on my child's multiple " issues " or take the time to

do the research. We inevitably must teach the doctors.

In saying that, a culmination of all their work has been very

helpful. For newbies, however, its a maze and very frustrating.

Where can one get the tests you outlined? Does IWDL do these kinds

of tests?

thank you

> > >

> > > ... I find it very odd that his findings and suggestions have

not

> > been

> > > explored by DAN! and others to greater extent!

> > >

> > > I have saved the text below a while ago, someone brought up

> > discussion

> > > on one of the treatments..

> > >

> > > here is a bit more on his work:

> > > http://www.latitudes.org/articles/singh_neuro_ts.html

> > >

> > >

> > > 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

> > >

> > > Autism is an early-onset biological disorder that causes severe

> > > deficits of higher mental functions, as well as behavioral

> > > manifestations. There is no single, clear-cut cause and no

> > complete

> > > cure for autism. Causally speaking, immune factors, neuro-

chemical

> > > factors, genetic susceptibility factors and environmental

factors

> > (such

> > > as microbial infections and chemical toxicity) have been

> > implicated. I

> > > view autism as a very complex, multifactorial disorder. In this

> > > article, I will attempt to describe succinctly the role of

> > autoimmune

> > > etiology and immune therapy for autism.

> > >

> > > As a neuroimmunologist, I have been interested in the

immunology

> > of the

> > > nervous system, i.e., the immune basis and immune therapy for

> > brain

> > > diseases and mental illnesses. I have studied autism as an

> > autoimmune

> > > disorder for over fifteen years. As a result, 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. I recently

postulated a

> > > " Neuroautoimmunity Model of Autism " which I discussed at two

> > recent

> > > conferences: first, the Biomedical Treatments for Autism and

PDD

> > > Conference held in Orlando, Florida (May, 1999); and second,

the

> > > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

> > Bethesda,

> > > land (June, 1999). Briefly, I hypothesized that an

autoimmune

> > > reaction to brain structures, in particular the myelin sheath,

> > plays a

> > > critical role in causing the neurological impairments of

patients

> > with

> > > autism. I 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.

> > >

> > > I believe that autism can be treated successfully using some of

> > the

> > > therapies proven effective in treating other autoimmune

diseases.

> > I am

> > > exploring specifically the role of autoimmune factors, (e.g.,

> > viruses,

> > > autoantibodies, T cells, and cytokines) because they serve as

the

> > prime

> > > targets of therapy with immune-modulating agents. I emphasize

the

> > need

> > > to focus on immunotherapies, and I urge doctors toexamine

> > autoimmunity

> > > as a novel target on which to focus in treating autistic

patients.

> > > There is enormous potential for restoring brain function in

> > autistic

> > > children and adults through immunology.

> > >

> > > Autoimmune Etiology in Autism

> > >

> > > A disease is commonly 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.

While

> > some

> > > of the key features are listed below, I will focus more on the

> > current

> > > research relating to three topics: viral studies; autoimmune

> > testing;

> > > and autoimmune therapy. 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, extended haplotypes,

etc.

> > >

> > > 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 respond well to immune therapies.

> > >

> > > Viral Studies in Autism

> > >

> > > Viruses have been linked to autism, but this relationship is

far

> > from

> > > fully explored. 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 was 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 never been investigated, I

think

> > this

> > > is due to a defect in T lymphocytes-these agents of immune

> > response are

> > > not functioning properly in these children. In an unpublished

> > pilot

> > > study, I found that the RV-induced lymphocyte proliferation

> > response in

> > > autistic children was only one-fourth of the response in normal

> > > children, which clearly suggests a defect of T cell-mediated

> > immunity

> > > (a defense mechanism that helps fight virus infections).

> > >

> > > 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. A few

> > years

> > > ago I and coworkers conducted a study of IgG antibodies to

CMV; we

> > > found no statistical difference between autistic children and

> > normal

> > > children (V. Singh, D. Schubert and R. Warren, 1992;

unpublished

> > data).

> > > Simply put, this means that CMV is probably not related to

autism.

> > >

> > > More recently, I conducted a study of measles virus (MV) and

human

> > > herpesvirus-6 (HHV-6) in autism. This was done by two types of

> > > laboratory analysis: (a) virus antibody levels of MV and HHV-6;

> > and (

> > > brain autoantibody titers in the same samples as those assayed

for

> > > virus antibodies. 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

> > 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 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.

> > >

> > > Testing for Autoimmunity in Autism

> > >

> > > Recent advances have clearly shown that autoimmunity plays a

key

> > role

> > > in the pathogenesis of autism. Since the brain is the affected

> > organ in

> > > autism, the autoimmune response will be directed against this

> > organ.

> > > This response is commonly identified by certain autoimmune

factors

> > > which I have identified in autistic children. The list includes

> > > brain-specific autoantibodies, viral antibodies, cytokine

profile

> > or

> > > immune activation markers, as well as antinuclear antibodies.

> > > Collectively, they are essential for identifying a brain-

specific

> > > autoimmune response, which can afterward be treated with immune

> > > therapy. By performing blood tests we can determine if a

patient

> > shows

> > > autoimmunity to brain tissues, if he or she is a candidate for

> > > experimental immune therapy, and if the response to therapy is

> > > effective. Therefore, this type of immune evaluation is very

> > important

> > > in helping children with autism.

> > >

> > > Brain autoantibodies: this test detects antibodies to two brain

> > > proteins, namely 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. It is, however, recommended that the

two

> > > markers be tested simultaneously.

> > >

> > > Cytokine profile: 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: this test 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: this test assays for antinuclear

> > antibodies

> > > (ANA). They are non-specific antibodies but are often present

in

> > > patients with autoimmune diseases. Approximately one-third of

> > autistic

> > > children tested have positive titers of ANA (V. Singh, 1992;

> > > unpublished data).

> > >

> > > Immunotherapy in Autism

> > >

> > > The aforementioned laboratory findings clearly point to an

> > autoimmune

> > > pathogenic mechanism in autism. The idea that autism is an

> > autoimmune

> > > disorder is further strengthened by the fact that autistic

> > patients

> > > respond well to treatment with immune modulating drugs. Immune

> > > interventions can produce immune modulation-a state of

suppression

> > or

> > > stimulation. Depending on the nature of the immune abnormality,

> > 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. Immune therapy should always be done in

> > consultation

> > > with physicians. The following immune interventions can be

used:

> > >

> > > Steroid therapy: steroids such as Prednisone and/or ACTH

> > > (adrenocorticotropin hormone) are commonly used as anti-

> > inflammatory

> > > and/or immunosuppressive drugs for treating patients with

> > autoimmune

> > > diseases, inflammatory diseases, etc. In autism, however, there

> > is only

> > > one study that showed improvement of autistic-like symptoms in

> > children

> > > when they were treated with an ACTH analogue. This result

> > indicated

> > > that steroids are potentially useful in alleviating clinical

> > symptoms

> > > of autism. Steroids are the first course of treatment for

> > patients with

> > > autoimmune diseases and infantile spasm; however, their

efficacy

> > has

> > > not been evaluated in autism.

> > >

> > > Intraveneous immunoglobulin (IVIG): this type of treatment has

> > been

> > > used to treat children with autism. Open-label trials of both

low-

> > dose

> > > and high-dose IVIG have shown that most but not all autistic

> > children

> > > respond favorably to this treatment. My collaborators and I

> > recently

> > > found that the high-dose IVIG was better than the low-dose IVIG

> > (J.

> > > Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> > > International Symposium on Autism, Netherlands, December 28-30,

> > 1999).

> > > Clinically, children so treated have shown improvements in

> > language,

> > > communication, social interaction and attention span. In a

double-

> > blind

> > > study, (V. Singh, 1997; unpublished data) the IVIG treatment

was

> > found

> > > to decrease brain autoantibody titers in five patients (they

were

> > > positive pre-therapy but became virtually negative post-

therapy)

> > who

> > > also showed clinical improvement of autistic characteristics.

In

> > spite

> > > of the success of IVIG, this treatment is not for everyone.

> > Before this

> > > treatment is administered, a proper immune evaluation is highly

> > > recommended to assess the nature of the immune problem.

> > >

> > > Oral tolerance with autoantigens: this treatment is a means of

> > inducing

> > > immune suppression by feeding patients autoantigen. I have

shown

> > that

> > > the candidate autoantigen in autism appeared to be a myelin

basic

> > > protein (MBP); this suggested that the MBP-containing myelin

> > products

> > > can be used to treat autistic patients. Indeed, one such

product

> > known

> > > as Sphingolin has been used with success. Recently, the

parents,

> > school

> > > psychologists, and other professionals have anecdotally

reported

> > > tremendous improvements of autistic symptoms in their children.

> > These

> > > reports are undoubtedly quite encouraging and promising, but a

> > > well-designed clinical trial is warranted.

> > >

> > > Plasmapheresis: although it is not commonly recommended, this

> > procedure

> > > is used for treating patients with infections, autoimmune

> > diseases,

> > > immune complex diseases, etc. Because this method removes

harmful

> > > substances (e.g., autoantibodies) from the blood, it is

> > considered a

> > > viable immune therapy. The method has been used to treat

certain

> > brain

> > > disorders, for example Rasmussen's encephalitis (RE) and

> > > obsessive-compulsive disorder (OCD), in which autoimmunity has

> > been

> > > implicated as a basis of the disorder. Plasmapheresis produced

> > positive

> > > responses in patients with these disorders, and the responses

> > were much

> > > better with plasmapheresis when compared to the IVIG treatment.

> > In each

> > > case, the benefit to the patient was associated with the

lowering

> > of

> > > the anti-neuronal antibody titers. Since autistic patients also

> > have

> > > positive titers of brain autoantibodies, they should also

respond

> > to

> > > plasmapheresis. Although this treatment has long been suggested

> > for use

> > > in autism (V. Singh, 1997), plasmapheresis has thus far not

been

> > tried

> > > in patients with this disorder.

> > >

> > > Conclusion

> > >

> > > The evidence is rapidly accumulating to suggest that autism is

an

> > > autoimmune disorder. The autoimmune response is most likely

> > directed

> > > against the brain myelin, perhaps secondary to a viral

infection.

> > > Measles virus is a candidate but other possibilities remain to

be

> > > explored. More importantly, the patients respond to treatment

with

> > > immune therapies. Therefore, I conclude that autoimmunity

> > offersstrong

> > > prospects for drug discovery and therapy for autism.

Naturally, it

> > > deserves prompt attention from all those who want to help

people

> > with

> > > autism.

> > >

> > > Selected Reading

> > >

> > > Singh, V. K., " Plasma Increase of Interleukin-12 and

Interferon-

> > gamma:

> > > Pathological Significance in Autism " (Journal of

Neuroimmunology,

> > vol.

> > > 66, pp. 143-145 [1996]).

> > >

> > > Singh, V. K., " Immunotherapy for Brain Diseases and Mental

> > Illnesses, "

> > > (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

> > >

> > > Singh, V. K., " Serological Association of Measles Virus and

Human

> > > Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

> > Immunology

> > > and Immunopathology, vol. 89, pp. 105-108 [1998]).

> > >

> > > Singh, V. K., " Autoimmunity and Neurologic Disorders "

(Latitudes,

> > vol.

> > > 4, pp. 5-11 [1999]).

> > >

> > > Dr. Singh received his doctorate from the University of British

> > > Columbia, Vancouver, Canada. His post-doctoral fellowship was

> > completed

> > > in neurochemistry and neuroimmunology. Spanning over twenty

years'

> > > experience in neurobiology and immunology research, Dr. Singh

> > studied

> > > brain diseases, particularly infantile autism and Alzheimer's

> > disease.

> > > Having authored over a hundred scientific publications, he is

both

> > a

> > > pioneer and an international authority on autoimmunity in

autism.

> > Dr.

> > > Singh is a member of the American Association for the

Advancement

> > of

> > > Sciences, the American Association of Immunologists, and the

New

> > York

> > > Academy of Sciences. He is listed in American Men and Women in

> > Science

> > > (United States, R. R. Bowker, publisher) and The International

> > Who's

> > > Who of Intellectuals (Cambridge, England, International

> > Biographical

> > > Centre).

> > >

> > > For further information, please contact Dr. Vijendra Singh,

Ph.D.,

> > at

> > > the Biotechnology Center, Department of Biology, Utah State

> > University,

> > > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> > > singhvk@].

> > >

> > > Reprinted from AAPN, The Autism Autoimmunity Project

Newsletter,

> > vol. 1,

> > > number 2, December 1999.

> > >

> > >

> > >

> > > Links

> > >

> > > " Autoimmunity and Neurological Disorders, " interview with V. K.

> > Singh in

> > > Latitudes, newsletter of the Association for

> > > Comprehensive NeuroTherapy,

http://www.latitudes.org/index.html,

> > vol. 4,

> > > no. 2, Spring 1999, by Sheila

> > > : http://lib.tcu.edu/www/staff/lruede/latitudes

> > >

> > > " V. K. Singh: Selected Research on Autism, "

> > http://www.gti.net/truegrit/

> > > : Findings in Immunology

> > >

> > > " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's

Disease, "

> > > (http://lib.tcu.edu/www/staff/lruede/alzheimers)

> > >

> > >

> > >

> > >

> > > > __________________________________________________

> > > > Correo Yahoo!

> > > > Espacio para todos tus mensajes, antivirus y antispam

¡gratis!

> > > > Regístrate ya - http://correo.espanol.yahoo.com/

> > > >

> > >

> >

>

[Guest guest]

By single approach I mean he is looking only at the immune system as a cause and treatment for ASD. The problem with his approach is that there are plenty of ASD kids *without* brain antibodies present who are still ASD so it cannot explain all the cases of ASD.

Again, there is mention of Dr. Singh and Sphingolin in Dr. McCandless' *first* book way back in 2000. It was not found to be effective for any more than a very, very tiny subset of children, again, priceless if it were your child.

My main point is that there is no single cause or tx for ASD.

Re: Autism tests and treatments - recommened by Dr Singh

On the contrary , this is anything BUT a single approach! Read abit on what this guy is actually saying as the opposite is actually thecase - his 'single' theory of ASD etiology (and recommended tests andeventual treatment options) is the most complex I have read to date.fwiw the fact that he skips some of the more common treatments is thathe may well be after the core problems, by the look of it.it could well be that it fell weyside as it is very complex and not manyDAN!s out there who have the necessary knowledge and expertise, ifanyone.natasa> >> > ... I find it very odd that his findings and suggestions have not> been> > explored by DAN! and others to greater extent!> >> > I have saved the text below a while ago, someone brought up> discussion> > on one of the treatments..> >> > here is a bit more on his work:> > http://www.latitudes.org/articles/singh_neuro_ts.html> >> >> > 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> >> > Autism is an early-onset biological disorder that causes severe> > deficits of higher mental functions, as well as behavioral> > manifestations. There is no single, clear-cut cause and no> complete> > cure for autism. Causally speaking, immune factors, neuro-chemical> > factors, genetic susceptibility factors and environmental factors> (such> > as microbial infections and chemical toxicity) have been> implicated. I> > view autism as a very complex, multifactorial disorder. In this> > article, I will attempt to describe succinctly the role of> autoimmune> > etiology and immune therapy for autism.> >> > As a neuroimmunologist, I have been interested in the immunology> of the> > nervous system, i.e., the immune basis and immune therapy for> brain> > diseases and mental illnesses. I have studied autism as an> autoimmune> > disorder for over fifteen years. As a result, 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. I recently postulated a> > "Neuroautoimmunity Model of Autism" which I discussed at two> recent> > conferences: first, the Biomedical Treatments for Autism and PDD> > Conference held in Orlando, Florida (May, 1999); and second, the> > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in> Bethesda,> > land (June, 1999). Briefly, I hypothesized that an autoimmune> > reaction to brain structures, in particular the myelin sheath,> plays a> > critical role in causing the neurological impairments of patients> with> > autism. I 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.> >> > I believe that autism can be treated successfully using some of> the> > therapies proven effective in treating other autoimmune diseases.> I am> > exploring specifically the role of autoimmune factors, (e.g.,> viruses,> > autoantibodies, T cells, and cytokines) because they serve as the> prime> > targets of therapy with immune-modulating agents. I emphasize the> need> > to focus on immunotherapies, and I urge doctors toexamine> autoimmunity> > as a novel target on which to focus in treating autistic patients.> > There is enormous potential for restoring brain function in> autistic> > children and adults through immunology.> >> > Autoimmune Etiology in Autism> >> > A disease is commonly 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. While> some> > of the key features are listed below, I will focus more on the> current> > research relating to three topics: viral studies; autoimmune> testing;> > and autoimmune therapy. 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, extended haplotypes, etc.> >> > 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 respond well to immune therapies.> >> > Viral Studies in Autism> >> > Viruses have been linked to autism, but this relationship is far> from> > fully explored. 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 was 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 never been investigated, I think> this> > is due to a defect in T lymphocytes-these agents of immune> response are> > not functioning properly in these children. In an unpublished> pilot> > study, I found that the RV-induced lymphocyte proliferation> response in> > autistic children was only one-fourth of the response in normal> > children, which clearly suggests a defect of T cell-mediated> immunity> > (a defense mechanism that helps fight virus infections).> >> > 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. A few> years> > ago I and coworkers conducted a study of IgG antibodies to CMV; we> > found no statistical difference between autistic children and> normal> > children (V. Singh, D. Schubert and R. Warren, 1992; unpublished> data).> > Simply put, this means that CMV is probably not related to autism.> >> > More recently, I conducted a study of measles virus (MV) and human> > herpesvirus-6 (HHV-6) in autism. This was done by two types of> > laboratory analysis: (a) virus antibody levels of MV and HHV-6;> and (> > brain autoantibody titers in the same samples as those assayed for> > virus antibodies. 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> 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 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.> >> > Testing for Autoimmunity in Autism> >> > Recent advances have clearly shown that autoimmunity plays a key> role> > in the pathogenesis of autism. Since the brain is the affected> organ in> > autism, the autoimmune response will be directed against this> organ.> > This response is commonly identified by certain autoimmune factors> > which I have identified in autistic children. The list includes> > brain-specific autoantibodies, viral antibodies, cytokine profile> or> > immune activation markers, as well as antinuclear antibodies.> > Collectively, they are essential for identifying a brain-specific> > autoimmune response, which can afterward be treated with immune> > therapy. By performing blood tests we can determine if a patient> shows> > autoimmunity to brain tissues, if he or she is a candidate for> > experimental immune therapy, and if the response to therapy is> > effective. Therefore, this type of immune evaluation is very> important> > in helping children with autism.> >> > Brain autoantibodies: this test detects antibodies to two brain> > proteins, namely 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. It is, however, recommended that the two> > markers be tested simultaneously.> >> > Cytokine profile: 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: this test 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: this test assays for antinuclear> antibodies> > (ANA). They are non-specific antibodies but are often present in> > patients with autoimmune diseases. Approximately one-third of> autistic> > children tested have positive titers of ANA (V. Singh, 1992;> > unpublished data).> >> > Immunotherapy in Autism> >> > The aforementioned laboratory findings clearly point to an> autoimmune> > pathogenic mechanism in autism. The idea that autism is an> autoimmune> > disorder is further strengthened by the fact that autistic> patients> > respond well to treatment with immune modulating drugs. Immune> > interventions can produce immune modulation-a state of suppression> or> > stimulation. Depending on the nature of the immune abnormality,> 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. Immune therapy should always be done in> consultation> > with physicians. The following immune interventions can be used:> >> > Steroid therapy: steroids such as Prednisone and/or ACTH> > (adrenocorticotropin hormone) are commonly used as anti-> inflammatory> > and/or immunosuppressive drugs for treating patients with> autoimmune> > diseases, inflammatory diseases, etc. In autism, however, there> is only> > one study that showed improvement of autistic-like symptoms in> children> > when they were treated with an ACTH analogue. This result> indicated> > that steroids are potentially useful in alleviating clinical> symptoms> > of autism. Steroids are the first course of treatment for> patients with> > autoimmune diseases and infantile spasm; however, their efficacy> has> > not been evaluated in autism.> >> > Intraveneous immunoglobulin (IVIG): this type of treatment has> been> > used to treat children with autism. Open-label trials of both low-> dose> > and high-dose IVIG have shown that most but not all autistic> children> > respond favorably to this treatment. My collaborators and I> recently> > found that the high-dose IVIG was better than the low-dose IVIG> (J.> > Bradstreet, V. Singh and J. El-Dahr, paper presented at the> > International Symposium on Autism, Netherlands, December 28-30,> 1999).> > Clinically, children so treated have shown improvements in> language,> > communication, social interaction and attention span. In a double-> blind> > study, (V. Singh, 1997; unpublished data) the IVIG treatment was> found> > to decrease brain autoantibody titers in five patients (they were> > positive pre-therapy but became virtually negative post-therapy)> who> > also showed clinical improvement of autistic characteristics. In> spite> > of the success of IVIG, this treatment is not for everyone.> Before this> > treatment is administered, a proper immune evaluation is highly> > recommended to assess the nature of the immune problem.> >> > Oral tolerance with autoantigens: this treatment is a means of> inducing> > immune suppression by feeding patients autoantigen. I have shown> that> > the candidate autoantigen in autism appeared to be a myelin basic> > protein (MBP); this suggested that the MBP-containing myelin> products> > can be used to treat autistic patients. Indeed, one such product> known> > as Sphingolin has been used with success. Recently, the parents,> school> > psychologists, and other professionals have anecdotally reported> > tremendous improvements of autistic symptoms in their children.> These> > reports are undoubtedly quite encouraging and promising, but a> > well-designed clinical trial is warranted.> >> > Plasmapheresis: although it is not commonly recommended, this> procedure> > is used for treating patients with infections, autoimmune> diseases,> > immune complex diseases, etc. Because this method removes harmful> > substances (e.g., autoantibodies) from the blood, it is> considered a> > viable immune therapy. The method has been used to treat certain> brain> > disorders, for example Rasmussen's encephalitis (RE) and> > obsessive-compulsive disorder (OCD), in which autoimmunity has> been> > implicated as a basis of the disorder. Plasmapheresis produced> positive> > responses in patients with these disorders, and the responses> were much> > better with plasmapheresis when compared to the IVIG treatment.> In each> > case, the benefit to the patient was associated with the lowering> of> > the anti-neuronal antibody titers. Since autistic patients also> have> > positive titers of brain autoantibodies, they should also respond> to> > plasmapheresis. Although this treatment has long been suggested> for use> > in autism (V. Singh, 1997), plasmapheresis has thus far not been> tried> > in patients with this disorder.> >> > Conclusion> >> > The evidence is rapidly accumulating to suggest that autism is an> > autoimmune disorder. The autoimmune response is most likely> directed> > against the brain myelin, perhaps secondary to a viral infection.> > Measles virus is a candidate but other possibilities remain to be> > explored. More importantly, the patients respond to treatment with> > immune therapies. Therefore, I conclude that autoimmunity> offersstrong> > prospects for drug discovery and therapy for autism. Naturally, it> > deserves prompt attention from all those who want to help people> with> > autism.> >> > Selected Reading> >> > Singh, V. K., "Plasma Increase of Interleukin-12 and Interferon-> gamma:> > Pathological Significance in Autism" (Journal of Neuroimmunology,> vol.> > 66, pp. 143-145 [1996]).> >> > Singh, V. K., "Immunotherapy for Brain Diseases and Mental> Illnesses,"> > (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).> >> > Singh, V. K., "Serological Association of Measles Virus and Human> > Herpesvirus-6 With Brain Autoantibodies in Autism" (Clinical> Immunology> > and Immunopathology, vol. 89, pp. 105-108 [1998]).> >> > Singh, V. K., "Autoimmunity and Neurologic Disorders" (Latitudes,> vol.> > 4, pp. 5-11 [1999]).> >> > Dr. Singh received his doctorate from the University of British> > Columbia, Vancouver, Canada. His post-doctoral fellowship was> completed> > in neurochemistry and neuroimmunology. Spanning over twenty years'> > experience in neurobiology and immunology research, Dr. Singh> studied> > brain diseases, particularly infantile autism and Alzheimer's> disease.> > Having authored over a hundred scientific publications, he is both> a> > pioneer and an international authority on autoimmunity in autism.> Dr.> > Singh is a member of the American Association for the Advancement> of> > Sciences, the American Association of Immunologists, and the New> York> > Academy of Sciences. He is listed in American Men and Women in> Science> > (United States, R. R. Bowker, publisher) and The International> Who's> > Who of Intellectuals (Cambridge, England, International> Biographical> > Centre).> >> > For further information, please contact Dr. Vijendra Singh, Ph.D.,> at> > the Biotechnology Center, Department of Biology, Utah State> University,> > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:> > singhvk@].> >> > Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,> vol. 1,> > number 2, December 1999.> >> >> >> > Links> >> > "Autoimmunity and Neurological Disorders," interview with V. K.> Singh in> > Latitudes, newsletter of the Association for> > Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,> vol. 4,> > no. 2, Spring 1999, by Sheila> > : http://lib.tcu.edu/www/staff/lruede/latitudes> >> > "V. K. Singh: Selected Research on Autism,"> http://www.gti.net/truegrit/> > : Findings in Immunology> >> > "Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease,"> > (http://lib.tcu.edu/www/staff/lruede/alzheimers)> >> >> >> >> > > __________________________________________________> > > Correo Yahoo!> > > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!> > > Regístrate ya - http://correo.espanol.yahoo.com/> > >> >>

[Guest guest]

Sphingolin is available via the yasko website Holistic Heal. I just

bought and am about to try. Maybe Mandi would consider adding to her

website???

Bests

gail

> >

> > ... I find it very odd that his findings and suggestions have

not

> been

> > explored by DAN! and others to greater extent!

> >

> > I have saved the text below a while ago, someone brought up

> discussion

> > on one of the treatments..

> >

> > here is a bit more on his work:

> > http://www.latitudes.org/articles/singh_neuro_ts.html

> >

> >

> > 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

> >

> > Autism is an early-onset biological disorder that causes severe

> > deficits of higher mental functions, as well as behavioral

> > manifestations. There is no single, clear-cut cause and no

> complete

> > cure for autism. Causally speaking, immune factors, neuro-

chemical

> > factors, genetic susceptibility factors and environmental

factors

> (such

> > as microbial infections and chemical toxicity) have been

> implicated. I

> > view autism as a very complex, multifactorial disorder. In this

> > article, I will attempt to describe succinctly the role of

> autoimmune

> > etiology and immune therapy for autism.

> >

> > As a neuroimmunologist, I have been interested in the immunology

> of the

> > nervous system, i.e., the immune basis and immune therapy for

> brain

> > diseases and mental illnesses. I have studied autism as an

> autoimmune

> > disorder for over fifteen years. As a result, 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. I recently postulated

a

> > " Neuroautoimmunity Model of Autism " which I discussed at two

> recent

> > conferences: first, the Biomedical Treatments for Autism and PDD

> > Conference held in Orlando, Florida (May, 1999); and second, the

> > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

> Bethesda,

> > land (June, 1999). Briefly, I hypothesized that an

autoimmune

> > reaction to brain structures, in particular the myelin sheath,

> plays a

> > critical role in causing the neurological impairments of

patients

> with

> > autism. I 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.

> >

> > I believe that autism can be treated successfully using some of

> the

> > therapies proven effective in treating other autoimmune

diseases.

> I am

> > exploring specifically the role of autoimmune factors, (e.g.,

> viruses,

> > autoantibodies, T cells, and cytokines) because they serve as

the

> prime

> > targets of therapy with immune-modulating agents. I emphasize

the

> need

> > to focus on immunotherapies, and I urge doctors toexamine

> autoimmunity

> > as a novel target on which to focus in treating autistic

patients.

> > There is enormous potential for restoring brain function in

> autistic

> > children and adults through immunology.

> >

> > Autoimmune Etiology in Autism

> >

> > A disease is commonly 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.

While

> some

> > of the key features are listed below, I will focus more on the

> current

> > research relating to three topics: viral studies; autoimmune

> testing;

> > and autoimmune therapy. 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, extended haplotypes, etc.

> >

> > 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 respond well to immune therapies.

> >

> > Viral Studies in Autism

> >

> > Viruses have been linked to autism, but this relationship is far

> from

> > fully explored. 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 was 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 never been investigated, I think

> this

> > is due to a defect in T lymphocytes-these agents of immune

> response are

> > not functioning properly in these children. In an unpublished

> pilot

> > study, I found that the RV-induced lymphocyte proliferation

> response in

> > autistic children was only one-fourth of the response in normal

> > children, which clearly suggests a defect of T cell-mediated

> immunity

> > (a defense mechanism that helps fight virus infections).

> >

> > 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. A few

> years

> > ago I and coworkers conducted a study of IgG antibodies to CMV;

we

> > found no statistical difference between autistic children and

> normal

> > children (V. Singh, D. Schubert and R. Warren, 1992; unpublished

> data).

> > Simply put, this means that CMV is probably not related to

autism.

> >

> > More recently, I conducted a study of measles virus (MV) and

human

> > herpesvirus-6 (HHV-6) in autism. This was done by two types of

> > laboratory analysis: (a) virus antibody levels of MV and HHV-6;

> and (

> > brain autoantibody titers in the same samples as those assayed

for

> > virus antibodies. 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

> 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 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.

> >

> > Testing for Autoimmunity in Autism

> >

> > Recent advances have clearly shown that autoimmunity plays a key

> role

> > in the pathogenesis of autism. Since the brain is the affected

> organ in

> > autism, the autoimmune response will be directed against this

> organ.

> > This response is commonly identified by certain autoimmune

factors

> > which I have identified in autistic children. The list includes

> > brain-specific autoantibodies, viral antibodies, cytokine

profile

> or

> > immune activation markers, as well as antinuclear antibodies.

> > Collectively, they are essential for identifying a brain-

specific

> > autoimmune response, which can afterward be treated with immune

> > therapy. By performing blood tests we can determine if a patient

> shows

> > autoimmunity to brain tissues, if he or she is a candidate for

> > experimental immune therapy, and if the response to therapy is

> > effective. Therefore, this type of immune evaluation is very

> important

> > in helping children with autism.

> >

> > Brain autoantibodies: this test detects antibodies to two brain

> > proteins, namely 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. It is, however, recommended that the two

> > markers be tested simultaneously.

> >

> > Cytokine profile: 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: this test 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: this test assays for antinuclear

> antibodies

> > (ANA). They are non-specific antibodies but are often present in

> > patients with autoimmune diseases. Approximately one-third of

> autistic

> > children tested have positive titers of ANA (V. Singh, 1992;

> > unpublished data).

> >

> > Immunotherapy in Autism

> >

> > The aforementioned laboratory findings clearly point to an

> autoimmune

> > pathogenic mechanism in autism. The idea that autism is an

> autoimmune

> > disorder is further strengthened by the fact that autistic

> patients

> > respond well to treatment with immune modulating drugs. Immune

> > interventions can produce immune modulation-a state of

suppression

> or

> > stimulation. Depending on the nature of the immune abnormality,

> 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. Immune therapy should always be done in

> consultation

> > with physicians. The following immune interventions can be used:

> >

> > Steroid therapy: steroids such as Prednisone and/or ACTH

> > (adrenocorticotropin hormone) are commonly used as anti-

> inflammatory

> > and/or immunosuppressive drugs for treating patients with

> autoimmune

> > diseases, inflammatory diseases, etc. In autism, however, there

> is only

> > one study that showed improvement of autistic-like symptoms in

> children

> > when they were treated with an ACTH analogue. This result

> indicated

> > that steroids are potentially useful in alleviating clinical

> symptoms

> > of autism. Steroids are the first course of treatment for

> patients with

> > autoimmune diseases and infantile spasm; however, their

efficacy

> has

> > not been evaluated in autism.

> >

> > Intraveneous immunoglobulin (IVIG): this type of treatment has

> been

> > used to treat children with autism. Open-label trials of both

low-

> dose

> > and high-dose IVIG have shown that most but not all autistic

> children

> > respond favorably to this treatment. My collaborators and I

> recently

> > found that the high-dose IVIG was better than the low-dose IVIG

> (J.

> > Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> > International Symposium on Autism, Netherlands, December 28-30,

> 1999).

> > Clinically, children so treated have shown improvements in

> language,

> > communication, social interaction and attention span. In a

double-

> blind

> > study, (V. Singh, 1997; unpublished data) the IVIG treatment

was

> found

> > to decrease brain autoantibody titers in five patients (they

were

> > positive pre-therapy but became virtually negative post-

therapy)

> who

> > also showed clinical improvement of autistic characteristics.

In

> spite

> > of the success of IVIG, this treatment is not for everyone.

> Before this

> > treatment is administered, a proper immune evaluation is highly

> > recommended to assess the nature of the immune problem.

> >

> > Oral tolerance with autoantigens: this treatment is a means of

> inducing

> > immune suppression by feeding patients autoantigen. I have shown

> that

> > the candidate autoantigen in autism appeared to be a myelin

basic

> > protein (MBP); this suggested that the MBP-containing myelin

> products

> > can be used to treat autistic patients. Indeed, one such product

> known

> > as Sphingolin has been used with success. Recently, the

parents,

> school

> > psychologists, and other professionals have anecdotally reported

> > tremendous improvements of autistic symptoms in their children.

> These

> > reports are undoubtedly quite encouraging and promising, but a

> > well-designed clinical trial is warranted.

> >

> > Plasmapheresis: although it is not commonly recommended, this

> procedure

> > is used for treating patients with infections, autoimmune

> diseases,

> > immune complex diseases, etc. Because this method removes

harmful

> > substances (e.g., autoantibodies) from the blood, it is

> considered a

> > viable immune therapy. The method has been used to treat

certain

> brain

> > disorders, for example Rasmussen's encephalitis (RE) and

> > obsessive-compulsive disorder (OCD), in which autoimmunity has

> been

> > implicated as a basis of the disorder. Plasmapheresis produced

> positive

> > responses in patients with these disorders, and the responses

> were much

> > better with plasmapheresis when compared to the IVIG treatment.

> In each

> > case, the benefit to the patient was associated with the

lowering

> of

> > the anti-neuronal antibody titers. Since autistic patients also

> have

> > positive titers of brain autoantibodies, they should also

respond

> to

> > plasmapheresis. Although this treatment has long been suggested

> for use

> > in autism (V. Singh, 1997), plasmapheresis has thus far not

been

> tried

> > in patients with this disorder.

> >

> > Conclusion

> >

> > The evidence is rapidly accumulating to suggest that autism is

an

> > autoimmune disorder. The autoimmune response is most likely

> directed

> > against the brain myelin, perhaps secondary to a viral

infection.

> > Measles virus is a candidate but other possibilities remain to

be

> > explored. More importantly, the patients respond to treatment

with

> > immune therapies. Therefore, I conclude that autoimmunity

> offersstrong

> > prospects for drug discovery and therapy for autism. Naturally,

it

> > deserves prompt attention from all those who want to help people

> with

> > autism.

> >

> > Selected Reading

> >

> > Singh, V. K., " Plasma Increase of Interleukin-12 and Interferon-

> gamma:

> > Pathological Significance in Autism " (Journal of

Neuroimmunology,

> vol.

> > 66, pp. 143-145 [1996]).

> >

> > Singh, V. K., " Immunotherapy for Brain Diseases and Mental

> Illnesses, "

> > (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

> >

> > Singh, V. K., " Serological Association of Measles Virus and

Human

> > Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

> Immunology

> > and Immunopathology, vol. 89, pp. 105-108 [1998]).

> >

> > Singh, V. K., " Autoimmunity and Neurologic Disorders "

(Latitudes,

> vol.

> > 4, pp. 5-11 [1999]).

> >

> > Dr. Singh received his doctorate from the University of British

> > Columbia, Vancouver, Canada. His post-doctoral fellowship was

> completed

> > in neurochemistry and neuroimmunology. Spanning over twenty

years'

> > experience in neurobiology and immunology research, Dr. Singh

> studied

> > brain diseases, particularly infantile autism and Alzheimer's

> disease.

> > Having authored over a hundred scientific publications, he is

both

> a

> > pioneer and an international authority on autoimmunity in

autism.

> Dr.

> > Singh is a member of the American Association for the

Advancement

> of

> > Sciences, the American Association of Immunologists, and the New

> York

> > Academy of Sciences. He is listed in American Men and Women in

> Science

> > (United States, R. R. Bowker, publisher) and The International

> Who's

> > Who of Intellectuals (Cambridge, England, International

> Biographical

> > Centre).

> >

> > For further information, please contact Dr. Vijendra Singh,

Ph.D.,

> at

> > the Biotechnology Center, Department of Biology, Utah State

> University,

> > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> > singhvk@].

> >

> > Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,

> vol. 1,

> > number 2, December 1999.

> >

> >

> >

> > Links

> >

> > " Autoimmunity and Neurological Disorders, " interview with V. K.

> Singh in

> > Latitudes, newsletter of the Association for

> > Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,

> vol. 4,

> > no. 2, Spring 1999, by Sheila

> > : http://lib.tcu.edu/www/staff/lruede/latitudes

> >

> > " V. K. Singh: Selected Research on Autism, "

> http://www.gti.net/truegrit/

> > : Findings in Immunology

> >

> > " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's Disease, "

> > (http://lib.tcu.edu/www/staff/lruede/alzheimers)

> >

> >

> >

> >

> > > __________________________________________________

> > > Correo Yahoo!

> > > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > > Regístrate ya - http://correo.espanol.yahoo.com/

> > >

> >

>

[Guest guest]

Hi Natasa,

Oops yes - I think it was Dr Gupta. Was the mum Goldenberg

maybe.

Best wishes,

Sandy

> > >

> > > ... I find it very odd that his findings and suggestions have

not

> > been

> > > explored by DAN! and others to greater extent!

> > >

> > > I have saved the text below a while ago, someone brought up

> > discussion

> > > on one of the treatments..

> > >

> > > here is a bit more on his work:

> > > http://www.latitudes.org/articles/singh_neuro_ts.html

> > >

> > >

> > > 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

> > >

> > > Autism is an early-onset biological disorder that causes severe

> > > deficits of higher mental functions, as well as behavioral

> > > manifestations. There is no single, clear-cut cause and no

complete

> > > cure for autism. Causally speaking, immune factors, neuro-

chemical

> > > factors, genetic susceptibility factors and environmental

factors

> > (such

> > > as microbial infections and chemical toxicity) have been

> > implicated. I

> > > view autism as a very complex, multifactorial disorder. In this

> > > article, I will attempt to describe succinctly the role of

> > autoimmune

> > > etiology and immune therapy for autism.

> > >

> > > As a neuroimmunologist, I have been interested in the

immunology of

> > the

> > > nervous system, i.e., the immune basis and immune therapy for

brain

> > > diseases and mental illnesses. I have studied autism as an

> > autoimmune

> > > disorder for over fifteen years. As a result, 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. I recently postulated

a

> > > " Neuroautoimmunity Model of Autism " which I discussed at two

recent

> > > conferences: first, the Biomedical Treatments for Autism and PDD

> > > Conference held in Orlando, Florida (May, 1999); and second, the

> > > Neuro-Immune Dysfunction Syndromes (NIDS) Conference held in

> > Bethesda,

> > > land (June, 1999). Briefly, I hypothesized that an

autoimmune

> > > reaction to brain structures, in particular the myelin sheath,

> > plays a

> > > critical role in causing the neurological impairments of

patients

> > with

> > > autism. I 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.

> > >

> > > I believe that autism can be treated successfully using some of

the

> > > therapies proven effective in treating other autoimmune

diseases. I

> > am

> > > exploring specifically the role of autoimmune factors, (e.g.,

> > viruses,

> > > autoantibodies, T cells, and cytokines) because they serve as

the

> > prime

> > > targets of therapy with immune-modulating agents. I emphasize

the

> > need

> > > to focus on immunotherapies, and I urge doctors toexamine

> > autoimmunity

> > > as a novel target on which to focus in treating autistic

patients.

> > > There is enormous potential for restoring brain function in

> > autistic

> > > children and adults through immunology.

> > >

> > > Autoimmune Etiology in Autism

> > >

> > > A disease is commonly 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.

While

> > some

> > > of the key features are listed below, I will focus more on the

> > current

> > > research relating to three topics: viral studies; autoimmune

> > testing;

> > > and autoimmune therapy. 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, extended haplotypes, etc.

> > >

> > > 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 respond well to immune therapies.

> > >

> > > Viral Studies in Autism

> > >

> > > Viruses have been linked to autism, but this relationship is far

> > from

> > > fully explored. 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 was 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 never been investigated, I think

> > this

> > > is due to a defect in T lymphocytes-these agents of immune

response

> > are

> > > not functioning properly in these children. In an unpublished

pilot

> > > study, I found that the RV-induced lymphocyte proliferation

> > response in

> > > autistic children was only one-fourth of the response in normal

> > > children, which clearly suggests a defect of T cell-mediated

> > immunity

> > > (a defense mechanism that helps fight virus infections).

> > >

> > > 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. A few

> > years

> > > ago I and coworkers conducted a study of IgG antibodies to CMV;

we

> > > found no statistical difference between autistic children and

> > normal

> > > children (V. Singh, D. Schubert and R. Warren, 1992; unpublished

> > data).

> > > Simply put, this means that CMV is probably not related to

autism.

> > >

> > > More recently, I conducted a study of measles virus (MV) and

human

> > > herpesvirus-6 (HHV-6) in autism. This was done by two types of

> > > laboratory analysis: (a) virus antibody levels of MV and HHV-6;

and

> > (

> > > brain autoantibody titers in the same samples as those assayed

for

> > > virus antibodies. 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

> > 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 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.

> > >

> > > Testing for Autoimmunity in Autism

> > >

> > > Recent advances have clearly shown that autoimmunity plays a key

> > role

> > > in the pathogenesis of autism. Since the brain is the affected

> > organ in

> > > autism, the autoimmune response will be directed against this

> > organ.

> > > This response is commonly identified by certain autoimmune

factors

> > > which I have identified in autistic children. The list includes

> > > brain-specific autoantibodies, viral antibodies, cytokine

profile

> > or

> > > immune activation markers, as well as antinuclear antibodies.

> > > Collectively, they are essential for identifying a brain-

specific

> > > autoimmune response, which can afterward be treated with immune

> > > therapy. By performing blood tests we can determine if a patient

> > shows

> > > autoimmunity to brain tissues, if he or she is a candidate for

> > > experimental immune therapy, and if the response to therapy is

> > > effective. Therefore, this type of immune evaluation is very

> > important

> > > in helping children with autism.

> > >

> > > Brain autoantibodies: this test detects antibodies to two brain

> > > proteins, namely 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. It is, however, recommended that the two

> > > markers be tested simultaneously.

> > >

> > > Cytokine profile: 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: this test 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: this test assays for antinuclear

antibodies

> > > (ANA). They are non-specific antibodies but are often present

in

> > > patients with autoimmune diseases. Approximately one-third of

> > autistic

> > > children tested have positive titers of ANA (V. Singh, 1992;

> > > unpublished data).

> > >

> > > Immunotherapy in Autism

> > >

> > > The aforementioned laboratory findings clearly point to an

> > autoimmune

> > > pathogenic mechanism in autism. The idea that autism is an

> > autoimmune

> > > disorder is further strengthened by the fact that autistic

patients

> > > respond well to treatment with immune modulating drugs. Immune

> > > interventions can produce immune modulation-a state of

suppression

> > or

> > > stimulation. Depending on the nature of the immune abnormality,

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. Immune therapy should always be done in

> > consultation

> > > with physicians. The following immune interventions can be used:

> > >

> > > Steroid therapy: steroids such as Prednisone and/or ACTH

> > > (adrenocorticotropin hormone) are commonly used as anti-

> > inflammatory

> > > and/or immunosuppressive drugs for treating patients with

> > autoimmune

> > > diseases, inflammatory diseases, etc. In autism, however,

there is

> > only

> > > one study that showed improvement of autistic-like symptoms in

> > children

> > > when they were treated with an ACTH analogue. This result

indicated

> > > that steroids are potentially useful in alleviating clinical

> > symptoms

> > > of autism. Steroids are the first course of treatment for

patients

> > with

> > > autoimmune diseases and infantile spasm; however, their

efficacy

> > has

> > > not been evaluated in autism.

> > >

> > > Intraveneous immunoglobulin (IVIG): this type of treatment has

been

> > > used to treat children with autism. Open-label trials of both

low-

> > dose

> > > and high-dose IVIG have shown that most but not all autistic

> > children

> > > respond favorably to this treatment. My collaborators and I

> > recently

> > > found that the high-dose IVIG was better than the low-dose

IVIG (J.

> > > Bradstreet, V. Singh and J. El-Dahr, paper presented at the

> > > International Symposium on Autism, Netherlands, December 28-30,

> > 1999).

> > > Clinically, children so treated have shown improvements in

> > language,

> > > communication, social interaction and attention span. In a

double-

> > blind

> > > study, (V. Singh, 1997; unpublished data) the IVIG treatment

was

> > found

> > > to decrease brain autoantibody titers in five patients (they

were

> > > positive pre-therapy but became virtually negative post-

therapy)

> > who

> > > also showed clinical improvement of autistic characteristics.

In

> > spite

> > > of the success of IVIG, this treatment is not for everyone.

Before

> > this

> > > treatment is administered, a proper immune evaluation is highly

> > > recommended to assess the nature of the immune problem.

> > >

> > > Oral tolerance with autoantigens: this treatment is a means of

> > inducing

> > > immune suppression by feeding patients autoantigen. I have shown

> > that

> > > the candidate autoantigen in autism appeared to be a myelin

basic

> > > protein (MBP); this suggested that the MBP-containing myelin

> > products

> > > can be used to treat autistic patients. Indeed, one such product

> > known

> > > as Sphingolin has been used with success. Recently, the

parents,

> > school

> > > psychologists, and other professionals have anecdotally reported

> > > tremendous improvements of autistic symptoms in their children.

> > These

> > > reports are undoubtedly quite encouraging and promising, but a

> > > well-designed clinical trial is warranted.

> > >

> > > Plasmapheresis: although it is not commonly recommended, this

> > procedure

> > > is used for treating patients with infections, autoimmune

diseases,

> > > immune complex diseases, etc. Because this method removes

harmful

> > > substances (e.g., autoantibodies) from the blood, it is

considered

> > a

> > > viable immune therapy. The method has been used to treat

certain

> > brain

> > > disorders, for example Rasmussen's encephalitis (RE) and

> > > obsessive-compulsive disorder (OCD), in which autoimmunity has

been

> > > implicated as a basis of the disorder. Plasmapheresis produced

> > positive

> > > responses in patients with these disorders, and the responses

were

> > much

> > > better with plasmapheresis when compared to the IVIG

treatment. In

> > each

> > > case, the benefit to the patient was associated with the

lowering

> > of

> > > the anti-neuronal antibody titers. Since autistic patients also

> > have

> > > positive titers of brain autoantibodies, they should also

respond

> > to

> > > plasmapheresis. Although this treatment has long been suggested

> > for use

> > > in autism (V. Singh, 1997), plasmapheresis has thus far not

been

> > tried

> > > in patients with this disorder.

> > >

> > > Conclusion

> > >

> > > The evidence is rapidly accumulating to suggest that autism is

an

> > > autoimmune disorder. The autoimmune response is most likely

> > directed

> > > against the brain myelin, perhaps secondary to a viral

infection.

> > > Measles virus is a candidate but other possibilities remain to

be

> > > explored. More importantly, the patients respond to treatment

with

> > > immune therapies. Therefore, I conclude that autoimmunity

> > offersstrong

> > > prospects for drug discovery and therapy for autism. Naturally,

it

> > > deserves prompt attention from all those who want to help people

> > with

> > > autism.

> > >

> > > Selected Reading

> > >

> > > Singh, V. K., " Plasma Increase of Interleukin-12 and Interferon-

> > gamma:

> > > Pathological Significance in Autism " (Journal of

Neuroimmunology,

> > vol.

> > > 66, pp. 143-145 [1996]).

> > >

> > > Singh, V. K., " Immunotherapy for Brain Diseases and Mental

> > Illnesses, "

> > > (Progress in Drug Research, vol. 43, pp. 129-146 [1997]).

> > >

> > > Singh, V. K., " Serological Association of Measles Virus and

Human

> > > Herpesvirus-6 With Brain Autoantibodies in Autism " (Clinical

> > Immunology

> > > and Immunopathology, vol. 89, pp. 105-108 [1998]).

> > >

> > > Singh, V. K., " Autoimmunity and Neurologic Disorders "

(Latitudes,

> > vol.

> > > 4, pp. 5-11 [1999]).

> > >

> > > Dr. Singh received his doctorate from the University of British

> > > Columbia, Vancouver, Canada. His post-doctoral fellowship was

> > completed

> > > in neurochemistry and neuroimmunology. Spanning over twenty

years'

> > > experience in neurobiology and immunology research, Dr. Singh

> > studied

> > > brain diseases, particularly infantile autism and Alzheimer's

> > disease.

> > > Having authored over a hundred scientific publications, he is

both

> > a

> > > pioneer and an international authority on autoimmunity in

autism.

> > Dr.

> > > Singh is a member of the American Association for the

Advancement

> > of

> > > Sciences, the American Association of Immunologists, and the New

> > York

> > > Academy of Sciences. He is listed in American Men and Women in

> > Science

> > > (United States, R. R. Bowker, publisher) and The International

> > Who's

> > > Who of Intellectuals (Cambridge, England, International

> > Biographical

> > > Centre).

> > >

> > > For further information, please contact Dr. Vijendra Singh,

Ph.D.,

> > at

> > > the Biotechnology Center, Department of Biology, Utah State

> > University,

> > > 4700 Old Main Hill, Logan, UT 84322-4700 [E-mail:

> > > singhvk@].

> > >

> > > Reprinted from AAPN, The Autism Autoimmunity Project Newsletter,

> > vol. 1,

> > > number 2, December 1999.

> > >

> > >

> > >

> > > Links

> > >

> > > " Autoimmunity and Neurological Disorders, " interview with V. K.

> > Singh in

> > > Latitudes, newsletter of the Association for

> > > Comprehensive NeuroTherapy, http://www.latitudes.org/index.html,

> > vol. 4,

> > > no. 2, Spring 1999, by Sheila

> > > : http://lib.tcu.edu/www/staff/lruede/latitudes

> > >

> > > " V. K. Singh: Selected Research on Autism, "

> > http://www.gti.net/truegrit/

> > > : Findings in Immunology

> > >

> > > " Vijendra K. Singh, Ph.D.: Selected Work on Alzheimer's

Disease, "

> > > (http://lib.tcu.edu/www/staff/lruede/alzheimers)

> > >

> > >

> > >

> > >

> > > > __________________________________________________

> > > > Correo Yahoo!

> > > > Espacio para todos tus mensajes, antivirus y antispam ¡gratis!

> > > > Regístrate ya - http://correo.espanol.yahoo.com/

> > > >

> > >

> >

>

[Guest guest]

"...By single approach I mean he is looking only at the immune system as a cause and treatment for ASD...", that statement could not be more off the mark!!Immune system overactivation is to be looked as INTERCONNECTED with everything else! ... whether it is viruses or bacteria or mercury or pesticides or radiation or combination of any of those the immune system will react by upping the inflammatory messengers, which can in itself be doing harm. and more importantly still, if the immune system is pushed enough and if there is a lack of regulatory mechanism, it will at some point turn to attack the host body. which is where real mess starts.yes, not everyone has brain myelin antibodies. and some 'normal' people have them. but there are many many more antibodies that could well be present in some kids and could be doing mess, that have not been looked into.this is an area that desperately needs more research and funding and looking into, defining this as 'just' autoimmune theory is definitely not in order. especially as it could potentially explain and help more severe cases and non-responding kids.natasa

[Guest guest]

Natasa, its actually the most confusing part of autism and the most

revealing in my opinion. What is so frustrating is that as a parent

and for all the rest of us, we are on our own.

Like now, i have just discovered this info from you about Dr Singh,

and about what other people say about autism as an auto

immune " disease " but what do we do about it, without the doctors

help. As a parent, i can only go so far. I can just hear my son's GP

laugh in my face when i ask him for some directed tests.

We can of course get the mbp tests done, (have done so alredy) but

the real nitty gritty stuff, at least for us, is yet beyond our

reach (for a reason perhaps???)

I know in my heart that this is the " heart " of autism and nobody

wants to touch it with a barge pole except for a very few.

There is no point in following DAN or any other protocol on its own

without seeing the bigger picture and that calls for tests,

interpretation of tests and accessing the information to put it all

together.

I feel like what is going to help my son is always just out of

reach. I am sure many others feel this way too. We have gone as far

as we can right now, we need more info and more help. The answers

are there, but who wants to help us get them.

Makes me so very angry. Even the doctors we use who have been

helping us only know " so much " they dont have the time to spend on

my boy or talking with me. It would take weeks of dialogue to

discuss each child and get tests done and interpret, etc.

As a parent, all i can say to those new to this is read as much as

you possibly can and don't take anyone's word for your child and

dont stop till you find what you need and dont EVER take anyone's

experiences/approach for granted, that it might be good for your

child. The DAN protocol is like a recipe book and increasingly i am

feeling left out of the loop on it, it just doesnt offer us much.

whew, feel better getting that off my chest!

>

> " ...By single approach I mean he is looking only at the immune

system as

> a cause and treatment for ASD... "

>

> , that statement could not be more off the mark!!

>

>

> Immune system overactivation is to be looked as INTERCONNECTED with

> everything else! ... whether it is viruses or bacteria or

mercury or

> pesticides or radiation or combination of any of those the immune

> system will react by upping the inflammatory messengers, which can

in

> itself be doing harm.

>

> and more importantly still, if the immune system is pushed

enough and

> if there is a lack of regulatory mechanism, it will at some point

turn

> to attack the host body. which is where real mess starts.

>

> yes, not everyone has brain myelin antibodies. and some 'normal'

people

> have them. but there are many many more antibodies that could well

be

> present in some kids and could be doing mess, that have not been

looked

> into.

>

> this is an area that desperately needs more research and funding

and

> looking into, defining this as 'just' autoimmune theory is

definitely

> not in order. especially as it could potentially explain and help

more

> severe cases and non-responding kids.

>

> natasa

>

[Guest guest]

Dear Natasa,

As you know my son has not been a big responder, in spite of starting

biomedical before he was two, in spite of undertaking a great many

interventions that I beleived to be fairly safe. I believe that

autoimmunity issues hold some part of the answer for my son.

I have very little time for research right now, but it did occur to

me--and I really hesitate to say this for many reasons--that maybe

another very selective yahoo group would be of help here. The focus

would be entirely autoimmunity and membership would be limited to

only those who want to research and pull together ideas. Not just

show up and ask questions about their individual child. I would love

to see a files section that holds all of these ideas in one place. I

would love to participate in a group like this, where we explore this

important issue as a small but motivated collective (I foresee having

a bit more time--fingers crossed--in a little while). I believe you

would be the perfect moderator for this group.

Please don't hesitate to tell me I'm a presumptuous idiot for my

suggestion ;-)

Anita

>

> " ...By single approach I mean he is looking only at the immune

system as

> a cause and treatment for ASD... "

>

> , that statement could not be more off the mark!!

>

>

> Immune system overactivation is to be looked as INTERCONNECTED with

> everything else! ... whether it is viruses or bacteria or mercury

or

> pesticides or radiation or combination of any of those the immune

> system will react by upping the inflammatory messengers, which can

in

> itself be doing harm.

>

> and more importantly still, if the immune system is pushed enough

and

> if there is a lack of regulatory mechanism, it will at some point

turn

> to attack the host body. which is where real mess starts.

>

> yes, not everyone has brain myelin antibodies. and some 'normal'

people

> have them. but there are many many more antibodies that could well

be

> present in some kids and could be doing mess, that have not been

looked

> into.

>

> this is an area that desperately needs more research and funding and

> looking into, defining this as 'just' autoimmune theory is

definitely

> not in order. especially as it could potentially explain and help

more

> severe cases and non-responding kids.

>

> natasa

>

[Guest guest]

I second that!!!!

A more focussed " focus group " would be greatly welcomed here. If it

happens, let me know and please issue me an invite.

> >

> > " ...By single approach I mean he is looking only at the immune

> system as

> > a cause and treatment for ASD... "

> >

> > , that statement could not be more off the mark!!

> >

> >

> > Immune system overactivation is to be looked as INTERCONNECTED

with

> > everything else! ... whether it is viruses or bacteria or

mercury

> or

> > pesticides or radiation or combination of any of those the

immune

> > system will react by upping the inflammatory messengers, which

can

> in

> > itself be doing harm.

> >

> > and more importantly still, if the immune system is pushed

enough

> and

> > if there is a lack of regulatory mechanism, it will at some

point

> turn

> > to attack the host body. which is where real mess starts.

> >

> > yes, not everyone has brain myelin antibodies. and some 'normal'

> people

> > have them. but there are many many more antibodies that could

well

> be

> > present in some kids and could be doing mess, that have not been

> looked

> > into.

> >

> > this is an area that desperately needs more research and funding

and

> > looking into, defining this as 'just' autoimmune theory is

> definitely

> > not in order. especially as it could potentially explain and

help

> more

> > severe cases and non-responding kids.

> >

> > natasa

> >

>

[Guest guest]

Hi My daughter developed ITP 6 months after her MMR and went downhill rapidly from that point. I was told the ITP was caused by a virus, but after months of research found out that ITP was an autoimmune disease - I was told to look for the primary cause - autoimmune disease can be caused by mercury!!!! Anita wrote: Dear Natasa,As you know my son has not been a big responder, in spite of starting biomedical before he was two,

in spite of undertaking a great many interventions that I beleived to be fairly safe. I believe that autoimmunity issues hold some part of the answer for my son.I have very little time for research right now, but it did occur to me--and I really hesitate to say this for many reasons--that maybe another very selective yahoo group would be of help here. The focus would be entirely autoimmunity and membership would be limited to only those who want to research and pull together ideas. Not just show up and ask questions about their individual child. I would love to see a files section that holds all of these ideas in one place. I would love to participate in a group like this, where we explore this important issue as a small but motivated collective (I foresee having a bit more time--fingers crossed--in a little while). I believe you would be the perfect moderator for this group.Please don't hesitate to tell me

I'm a presumptuous idiot for my suggestion ;-)Anita>> "...By single approach I mean he is looking only at the immune system as> a cause and treatment for ASD..."> > , that statement could not be more off the mark!!> > > Immune system overactivation is to be looked as INTERCONNECTED with> everything else! ... whether it is viruses or bacteria or mercury or> pesticides or radiation or combination of any of those the immune> system will react by upping the inflammatory messengers, which can in> itself be doing harm.> > and more importantly still, if the immune system is pushed enough and> if there is a lack of regulatory mechanism, it will at some point turn>

to attack the host body. which is where real mess starts.> > yes, not everyone has brain myelin antibodies. and some 'normal' people> have them. but there are many many more antibodies that could well be> present in some kids and could be doing mess, that have not been looked> into.> > this is an area that desperately needs more research and funding and> looking into, defining this as 'just' autoimmune theory is definitely> not in order. especially as it could potentially explain and help more> severe cases and non-responding kids.> > natasa>

[Guest guest]

Natasa,

I would have missed this if I had not seen Anita's reply, somehow overlooking it.

We're just talking here right? Maybe I'm missing the point but I always thought that McCandless had all the parts (metals/autoimmunity/viruses) in mind when she talked about the immune system, but I didn't think that Goldberg and Singh do, they're strictly ASD is an autoimmune condition.

If you had them all in mind then I'm amiss but I didn't see anything in your messages to indicate that, particularly past posts, including your posts at Autism-Immune where the focus is not on metals, but autoimmunity and dysregulation of the immune system.

The dan! dr we went to at the end was strictly ASD is an autoimmune condition although, in our case it was apparent that metals were causing the autoimmunity/dysregulation as when they left so did the screwy immune parameters.

We are still doing things to support her immune system and I think she will be on Transfer Factor for a long, long time.

As I'm pretty sure I said, follow whatever lead you think leads to recovery. I wouldn't care if noone was behind the idea I thought critical to her recovery and in fact we proceeded with an idea that many thought was unwise only to find that it was the best way, for her. The people who love the child often know the best way.

Best to you,

Re: Autism tests and treatments - recommened by Dr Singh

Dear Natasa,As you know my son has not been a big responder, in spite of starting biomedical before he was two, in spite of undertaking a great many interventions that I beleived to be fairly safe. I believe that autoimmunity issues hold some part of the answer for my son.I have very little time for research right now, but it did occur to me--and I really hesitate to say this for many reasons--that maybe another very selective yahoo group would be of help here. The focus would be entirely autoimmunity and membership would be limited to only those who want to research and pull together ideas. Not just show up and ask questions about their individual child. I would love to see a files section that holds all of these ideas in one place. I would love to participate in a group like this, where we explore this important issue as a small but motivated collective (I foresee having a bit more time--fingers crossed--in a little while). I believe you would be the perfect moderator for this group.Please don't hesitate to tell me I'm a presumptuous idiot for my suggestion ;-)Anita>> "...By single approach I mean he is looking only at the immune system as> a cause and treatment for ASD..."> > , that statement could not be more off the mark!!> > > Immune system overactivation is to be looked as INTERCONNECTED with> everything else! ... whether it is viruses or bacteria or mercury or> pesticides or radiation or combination of any of those the immune> system will react by upping the inflammatory messengers, which can in> itself be doing harm.> > and more importantly still, if the immune system is pushed enough and> if there is a lack of regulatory mechanism, it will at some point turn> to attack the host body. which is where real mess starts.> > yes, not everyone has brain myelin antibodies. and some 'normal' people> have them. but there are many many more antibodies that could well be> present in some kids and could be doing mess, that have not been looked> into.> > this is an area that desperately needs more research and funding and> looking into, defining this as 'just' autoimmune theory is definitely> not in order. especially as it could potentially explain and help more> severe cases and non-responding kids.> > natasa>

[Guest guest]

--

hi

have you mentioned this to jean re the dr singh stuff? i recognise

you from the jean muscrfot site dont i?

- In Autism-Biomedical-Europe , " bbrowne123 "

wrote:

>

> Natasa, its actually the most confusing part of autism and the most

> revealing in my opinion. What is so frustrating is that as a parent

> and for all the rest of us, we are on our own.

>

> Like now, i have just discovered this info from you about Dr Singh,

> and about what other people say about autism as an auto

> immune " disease " but what do we do about it, without the doctors

> help. As a parent, i can only go so far. I can just hear my son's

GP

> laugh in my face when i ask him for some directed tests.

>

> We can of course get the mbp tests done, (have done so alredy) but

> the real nitty gritty stuff, at least for us, is yet beyond our

> reach (for a reason perhaps???)

>

> I know in my heart that this is the " heart " of autism and nobody

> wants to touch it with a barge pole except for a very few.

>

> There is no point in following DAN or any other protocol on its own

> without seeing the bigger picture and that calls for tests,

> interpretation of tests and accessing the information to put it all

> together.

>

> I feel like what is going to help my son is always just out of

> reach. I am sure many others feel this way too. We have gone as far

> as we can right now, we need more info and more help. The answers

> are there, but who wants to help us get them.

>

> Makes me so very angry. Even the doctors we use who have been

> helping us only know " so much " they dont have the time to spend on

> my boy or talking with me. It would take weeks of dialogue to

> discuss each child and get tests done and interpret, etc.

>

> As a parent, all i can say to those new to this is read as much as

> you possibly can and don't take anyone's word for your child and

> dont stop till you find what you need and dont EVER take anyone's

> experiences/approach for granted, that it might be good for your

> child. The DAN protocol is like a recipe book and increasingly i am

> feeling left out of the loop on it, it just doesnt offer us much.

>

> whew, feel better getting that off my chest!

>

>

> >

> > " ...By single approach I mean he is looking only at the immune

> system as

> > a cause and treatment for ASD... "

> >

> > , that statement could not be more off the mark!!

> >

> >

> > Immune system overactivation is to be looked as INTERCONNECTED

with

> > everything else! ... whether it is viruses or bacteria or

> mercury or

> > pesticides or radiation or combination of any of those the immune

> > system will react by upping the inflammatory messengers, which

can

> in

> > itself be doing harm.

> >

> > and more importantly still, if the immune system is pushed

> enough and

> > if there is a lack of regulatory mechanism, it will at some point

> turn

> > to attack the host body. which is where real mess starts.

> >

> > yes, not everyone has brain myelin antibodies. and some 'normal'

> people

> > have them. but there are many many more antibodies that could

well

> be

> > present in some kids and could be doing mess, that have not been

> looked

> > into.

> >

> > this is an area that desperately needs more research and funding

> and

> > looking into, defining this as 'just' autoimmune theory is

> definitely

> > not in order. especially as it could potentially explain and help

> more

> > severe cases and non-responding kids.

> >

> > natasa

> >

>

[Guest guest]

Hi, totally agree. Biggest problem here is that autoimmunity in general is a bit of a grey area. There are uncertainties even when it comes to some classified autoimmune diseases and there are rarely quick answers and treatments. One example is MS à it is known that there is excessive inflammation there (overactivation of the immune system - excessive production of cytokines) and that there is autoimmune pathology (=harmful antibodies that are actually produced by the person, not external in origin), but scientists are not sure how much of it IS actually pathological and how much just reactive. In other words the autobodies ARE present, but if you take them away/stop them from doing harm they donÕt know how much MS would actually still be MSÉ... the only thing known for sure is that chronic inflammation and immune activation are present, same as in autism really:http://en.wikipedia.org/wiki/Multiple_sclerosisalso see http://autoimmune.pathology.jhmi.edu/whatis_disease.cfmPardo et al autopsy study did not find infiltration of lymphocytes and autoantibodies in brains of autistic patients, which would 'disqualify' autism as autoimmune disease, but on the other hand various antibodies were often found in the blood and in the GI tractÉ there is also a possibility that some autoantibodies are affecting the brain indirectly, by affecting permeability of blood brain barrier or blood flow to the brainÉ Excessive levels of inflammatory cytokine Il-12 were also found in the blood in autism à incidentally it is one of the cytokines that is known to lead to development of autoimmunity. Inhibitory cytokine Il-10 is found to be very low in autism. this one is capable of stopping excessive production of those harmful cytokines, ones that can lead to autoimmunity (or be harmful just by being there). Vitamin D is also an inhibitor of those harmful cytokines, and this is thought to be the reason there is less MS (and autism?) in sunny parts of the world. It could be why some kids do well on high doses of CLO.. . fwiw I'm reading and looking into getting additional D from other sources, as recommended by VitDcouncil...Anita, I like the idea of a group, thanks IÕm not a good candidate as in a middle of looking for a new place and will be moving house soonish.. if there are any volunteers out there that would be great. I could forward whatever interesting bits I come across for the files.In the meantime there is another list you may be interested in http://health.groups.yahoo.com/group/Autism-Immune/ - not big on discussing treatments but lots of interesting files in there, and new research gets posted regularly Natasa x > >> > "...By single approach I mean he is looking only at the immune > system as> > a cause and treatment for ASD..."> > > > , that statement could not be more off the mark!!> > > > > > Immune system overactivation is to be looked as INTERCONNECTED with> > everything else! ... whether it is viruses or bacteria or > mercury or> > pesticides or radiation or combination of any of those the immune> > system will react by upping the inflammatory messengers, which can > in> > itself be doing harm.> > > > and more importantly still, if the immune system is pushed > enough and> > if there is a lack of regulatory mechanism, it will at some point > turn> > to attack the host body. which is where real mess starts.> > > > yes, not everyone has brain myelin antibodies. and some 'normal' > people> > have them. but there are many many more antibodies that could well > be> > present in some kids and could be doing mess, that have not been > looked> > into.> > > > this is an area that desperately needs more research and funding > and> > looking into, defining this as 'just' autoimmune theory is > definitely> > not in order. especially as it could potentially explain and help > more> > severe cases and non-responding kids.> > > > natasa> >>

[Guest guest]

Hi our DAn is treating Charlie for his immune system. The pterine

test from the French lab showing the neopterine and biopterine levels

are a marker of how out of kilter the immune system is. We were

giving spironalcton to lower neop and bh4 to raise biop. Now we are

using LDN to try to keep neop down. Have also used steroids when in

the States to reduce neop. These treatments have made a big

difference cognitively to Charlie. For mylein antibodies we used

actos for about 8 months. I don't think you can say that DAN is all

the same - depends on the dr.

Peta-

-- In Autism-Biomedical-Europe , " bbrowne123 "

wrote:

>

> Natasa, its actually the most confusing part of autism and the most

> revealing in my opinion. What is so frustrating is that as a parent

> and for all the rest of us, we are on our own.

>

> Like now, i have just discovered this info from you about Dr Singh,

> and about what other people say about autism as an auto

> immune " disease " but what do we do about it, without the doctors

> help. As a parent, i can only go so far. I can just hear my son's

GP

> laugh in my face when i ask him for some directed tests.

>

> We can of course get the mbp tests done, (have done so alredy) but

> the real nitty gritty stuff, at least for us, is yet beyond our

> reach (for a reason perhaps???)

>

> I know in my heart that this is the " heart " of autism and nobody

> wants to touch it with a barge pole except for a very few.

>

> There is no point in following DAN or any other protocol on its own

> without seeing the bigger picture and that calls for tests,

> interpretation of tests and accessing the information to put it all

> together.

>

> I feel like what is going to help my son is always just out of

> reach. I am sure many others feel this way too. We have gone as far

> as we can right now, we need more info and more help. The answers

> are there, but who wants to help us get them.

>

> Makes me so very angry. Even the doctors we use who have been

> helping us only know " so much " they dont have the time to spend on

> my boy or talking with me. It would take weeks of dialogue to

> discuss each child and get tests done and interpret, etc.

>

> As a parent, all i can say to those new to this is read as much as

> you possibly can and don't take anyone's word for your child and

> dont stop till you find what you need and dont EVER take anyone's

> experiences/approach for granted, that it might be good for your

> child. The DAN protocol is like a recipe book and increasingly i am

> feeling left out of the loop on it, it just doesnt offer us much.

>

> whew, feel better getting that off my chest!

>

>

> >

> > " ...By single approach I mean he is looking only at the immune

> system as

> > a cause and treatment for ASD... "

> >

> > , that statement could not be more off the mark!!

> >

> >

> > Immune system overactivation is to be looked as INTERCONNECTED

with

> > everything else! ... whether it is viruses or bacteria or

> mercury or

> > pesticides or radiation or combination of any of those the immune

> > system will react by upping the inflammatory messengers, which

can

> in

> > itself be doing harm.

> >

> > and more importantly still, if the immune system is pushed

> enough and

> > if there is a lack of regulatory mechanism, it will at some point

> turn

> > to attack the host body. which is where real mess starts.

> >

> > yes, not everyone has brain myelin antibodies. and some 'normal'

> people

> > have them. but there are many many more antibodies that could

well

> be

> > present in some kids and could be doing mess, that have not been

> looked

> > into.

> >

> > this is an area that desperately needs more research and funding

> and

> > looking into, defining this as 'just' autoimmune theory is

> definitely

> > not in order. especially as it could potentially explain and help

> more

> > severe cases and non-responding kids.

> >

> > natasa

> >

>

[Guest guest]

Hi Natasa

You put things very well and it makes alot of sense. I just wanted to

say that our dr is in Florida and it seems that in spite of the sunny

climate there appears to be plenty of autistic kids there - but alot

of it could be parents from all over the world!

Peta--

- In Autism-Biomedical-Europe , " natasa778 "

wrote:

>

> Hi, totally agree. Biggest problem here is that autoimmunity in

general

> is a bit of a grey area. There are uncertainties even when it

comes to

> some classified autoimmune diseases and there are rarely quick

answers

> and treatments. One example is MS à it is known that there is

> excessive inflammation there (overactivation of the immune system -

> excessive production of cytokines) and that there is autoimmune

> pathology (=harmful antibodies that are actually produced by the

person,

> not external in origin), but scientists are not sure how much of it

IS

> actually pathological and how much just reactive. In other words the

> autobodies ARE present, but if you take them away/stop them from

doing

> harm they donÕt know how much MS would actually still be MSÉ...

> the only thing known for sure is that chronic inflammation and

immune

> activation are present, same as in autism really:

>

> http://en.wikipedia.org/wiki/Multiple_sclerosis

>

> also see http://autoimmune.pathology.jhmi.edu/whatis_disease.cfm

>

> Pardo et al autopsy study did not find infiltration of lymphocytes

and

> autoantibodies in brains of autistic patients, which

would 'disqualify'

> autism as autoimmune disease, but on the other hand various

antibodies

> were often found in the blood and in the GI tractÉ there is also a

> possibility that some autoantibodies are affecting the brain

indirectly,

> by affecting permeability of blood brain barrier or blood flow to

the

> brainÉ

>

> Excessive levels of inflammatory cytokine Il-12 were also found in

the

> blood in autism à incidentally it is one of the cytokines that is

> known to lead to development of autoimmunity.

>

>

> Inhibitory cytokine Il-10 is found to be very low in autism. this

one is

> capable of stopping excessive production of those harmful cytokines,

> ones that can lead to autoimmunity (or be harmful just by being

there).

> Vitamin D is also an inhibitor of those harmful cytokines, and this

is

> thought to be the reason there is less MS (and autism?) in sunny

parts

> of the world. It could be why some kids do well on high doses of

CLO.. .

> fwiw I'm reading and looking into getting additional D from other

> sources, as recommended by VitDcouncil...

>

>

> Anita, I like the idea of a group, thanks IÕm not a good

> candidate as in a middle of looking for a new place and will be

moving

> house soonish.. if there are any volunteers out there that would be

> great. I could forward whatever interesting bits I come across for

the

> files.

> In the meantime there is another list you may be interested in

> http://health.groups.yahoo.com/group/Autism-Immune/ - not big on

> discussing treatments but lots of interesting files in there, and

new

> research gets posted regularly

>

> Natasa x

>

>

>

>

>

>

>

> > >

> > > " ...By single approach I mean he is looking only at the immune

> > system as

> > > a cause and treatment for ASD... "

> > >

> > > , that statement could not be more off the mark!!

> > >

> > >

> > > Immune system overactivation is to be looked as INTERCONNECTED

with

> > > everything else! ... whether it is viruses or bacteria or

> > mercury or

> > > pesticides or radiation or combination of any of those the

immune

> > > system will react by upping the inflammatory messengers, which

can

> > in

> > > itself be doing harm.

> > >

> > > and more importantly still, if the immune system is pushed

> > enough and

> > > if there is a lack of regulatory mechanism, it will at some

point

> > turn

> > > to attack the host body. which is where real mess starts.

> > >

> > > yes, not everyone has brain myelin antibodies. and some 'normal'

> > people

> > > have them. but there are many many more antibodies that could

well

> > be

> > > present in some kids and could be doing mess, that have not been

> > looked

> > > into.

> > >

> > > this is an area that desperately needs more research and funding

> > and

> > > looking into, defining this as 'just' autoimmune theory is

> > definitely

> > > not in order. especially as it could potentially explain and

help

> > more

> > > severe cases and non-responding kids.

> > >

> > > natasa

> > >

> >

>

[Guest guest]

I agree Peta, in the last 2-3 years most dans! have incorporated immune system testing and treatment into their protocol, largely I might say due to Jackie McCandless' insistence that the immune system is an important player in the dx.

And dare I say that almost every parent is aware of the importance of treating the two (immune system and metals) simultaneously with the vast improvement some had noted with antiviral treatment.

Also wanted to add that although we had improvement to NT with chelation we also used natural antiviral treatment (Virastop) with great improvements. Transfer Factor was also, in my mind, solely responsible for bringing her social development to normal, almost overnight and it has never waivered after appearing.

And we're not done. Just recently she was coming down with a minor upper respiratory infection. My dd picked up some Echinacea and with a day of giving it we got what is unmistakingly her normal viral treatment behavior. It is minor, but it's there.

Re: Autism tests and treatments - recommened by Dr Singh

Hi our DAn is treating Charlie for his immune system. The pterine test from the French lab showing the neopterine and biopterine levels are a marker of how out of kilter the immune system is. We were giving spironalcton to lower neop and bh4 to raise biop. Now we are using LDN to try to keep neop down. Have also used steroids when in the States to reduce neop. These treatments have made a big difference cognitively to Charlie. For mylein antibodies we used actos for about 8 months. I don't think you can say that DAN is all the same - depends on the dr.Peta> >> > "...By single approach I mean he is looking only at the immune > system as> > a cause and treatment for ASD..."> > > > , that statement could not be more off the mark!!> > > > > > Immune system overactivation is to be looked as INTERCONNECTED with> > everything else! ... whether it is viruses or bacteria or > mercury or> > pesticides or radiation or combination of any of those the immune> > system will react by upping the inflammatory messengers, which can > in> > itself be doing harm.> > > > and more importantly still, if the immune system is pushed > enough and> > if there is a lack of regulatory mechanism, it will at some point > turn> > to attack the host body. which is where real mess starts.> > > > yes, not everyone has brain myelin antibodies. and some 'normal' > people> > have them. but there are many many more antibodies that could well > be> > present in some kids and could be doing mess, that have not been > looked> > into.> > > > this is an area that desperately needs more research and funding > and> > looking into, defining this as 'just' autoimmune theory is > definitely> > not in order. especially as it could potentially explain and help > more> > severe cases and non-responding kids.> > > > natasa> >>