“Common Origin” for Autism and Schizophrenia?
December 17, 2008 by Kristina Chew, PhD
Filed under Health
What goes around, comes around.
1952. The DSM-I says this about “000-x28 Schizophrenic reaction, childhood type”:
Here will be classified those schizophrenic reactions occurring before puberty. The clinical picture may differ from schizophrenic reactions occurring in other age periods because of the immaturity and plasticity of the patient at the time of onset of the reaction. Psychotic reactions in children, manifesting primarily autism, will be classified here. [via Unstrange.com; my emphases]
And in 1968, in the DSM-II, here is the definition of “295.8 Schizophrenia, childhood type”:
This category is for cases in which schizophrenic symptoms appear before puberty. The condition may be manifested by autistic, atypical and withdrawn behavior; failure to develop identity separate from the mother’s; and general unevenness, gross immaturity and inadequacy of development. These developmental defects may result in mental retardation, which should also be diagnosed.[via Unstrange.com; my emphases]
Before autism was “autism” as we talk about it today, and before there was such a thing as “autism spectrum disorder,” autism was “childhood schizophrenia.” Now bring up autism and schizophrenia in the same conversation and you’ll get a heated response. Back in February, Dr. Nancy Minshew, Director of the University of Pittsburgh’s Center for Excellence in Autism Research, was quoted in the Pittsburgh Post-Gazette as saying that, in the past, some autistic children may have been mislabeled as schizophrenic, and placed in state hospitals or institutions; some (mis)interpreted her comments as somehow as suggesting that autistic children were schizophrenic, when Dr. Minshew was noting the differences in how we once classified and spoke about autism, in contrast to how we do today. Drawing on a new theory about autism and genetics, a November article suggested that autism and schizophrenia are the same disease.
A review of the research literature by developmental psychologist Annemie Ploeger suggests that autism and schizophrenia share a common origin. The review is from Ploeger’s doctoral thesis, “Towards an integration of evolutionary psychology and developmental science: New insights from evolutionary developmental biology” and is summarized in the December 16th Science Daily. Ploeger looked at whether there was a connection between autism and schizophrenia by focusing on the first month of pregnancy. She noted certain “physical abnormalities” in autistic children: “protruding ears,” “peculiar toes,” “a large head and intestinal problems.”
Ploeger’s research reveals that in the period between 20 and 40 days after fertilisation, the embryo is highly susceptible to disruptions. In this period, early organogenesis, there is a lot of interaction between the different parts of the body. If something goes wrong with a given part of the body, it greatly influences the development of other parts of the body. As people with schizophrenia and autism frequently have physical abnormalities to body parts formed during early organogenesis, Ploeger concluded that the foundation for these psychiatric disorders is laid very early during pregnancy.
The existence of a relationship between unhealthy behaviour during pregnancy and the subsequent development of schizophrenia and autism in the child was already known. However, Ploeger’s hypothesis that the early organogenesis stage is the most critical, is new. Ploeger bases her hypothesis on an extensive study of scientific literature in this area. She often had to make use of related studies; although a lot of research has been done into prenatal influences on the development of schizophrenia and autism, little is known about the influence that the period between 20 to 40 days after fertilisation has.
From this description, it’s not clear what sort of factors—the mother’s genetic make-up; any environmental agents—are seen as having an effect of early organogenesis, though “unhealthy behavior during pregnancy” of course suggests that the mother’s activities and behaviors are particularly under consideration here. Ploeger also notes that some women who took Softenon for morning sickness in the 1960s and 1970s gave birth to severely disabled children, as a result of taking the medicine: “Autistic children were born in four percent of pregnancies in which softenon was used, whereas normally this figure is 0.1 percent.”
This study, along with another noted on Monday about paternal age and children’s health, is focusing on how parents’ behaviors and decision (taking certain medications, having a child when one is older) can possibly have an impact on a child being autistic or not; on a child being “healthy” or not—-I’ll end by noting that I, and some other friends who have autistic children, followed all the recommendations about “how to have a healthy pregnancy” exactingly, and our husbands were younger than 40.
What comes around, comes around.
As I’ve said my husband and I will be 30 soon. Tristan is almost 6. I am very much a tea totaler, but I drank heavily at a party when I was either newly pregnant or not yet pregnant. Of was supposed to take up to a year and a half to get pregnant after depo. Took 3 months. I often worry if that caused it though my midwife assured me the baby would have miscarried if a problem was caused that early. I know I had a severe depression when pregnant with Tristan. And I craved veggies and could barely stomach meat, which is the opposite of my usual diet. I always wonder about his pregnancy. Mother blaming runs wild in our culture when it comes to the unborn. Many feel it’s a form of subjugation of women. My kids godmom says maybe his pregnancy was different because he was different, rather than vice versa.
I was 34 and 35, father is paranoid schizophrenic and I have learned that my kids have 50% of that happening in their teens/early 20s, which is when the Father developed it. I read a great book long ago on schizophrenia that talked about infantile autism and childhood schizophrenia. My review was picked up by some online sites. I willl have to come back and look at links.
This was definitely an interesting article, although I’m not sure I’m prepared yet to say that my stepson’s big ears caused his autism .
I like your last sentence – what comes around, comes around. Is that one of the stages of being an autistic parent – that at some point you realize and accept that life is what it is? The last few years I’ve found I’ve stopped buying a lot of books on autism and subscribing to magazines about autism. I obviously come here, because I really appreciate and enjoy your blog, but overall I don’t do nearly the internet searching on autism I used to.
I guess I’m less focused on data gathering and more focused on living life with my family because I think in the end life’s too short and you need to be picky about how you spend your time. Maybe that has less to do with a stage of autism and more with turning 40.
Anyway, thanks as always for sharing your ideas and thoughts. Reading your blog is something I look forward to each day.
Navi –
Each of my pregnancies was different than the other. With my first, I craved meat, vegetables and fruit and with my second I craved more traditional “comfort” foods – breads, pastas, cereal, etc. Interestingly, those are the food preferences that my two youngest girls show.
I think your child’s godmother was right – his pregnancy was unique to him. I think most pregnancies are, truth be told. I think it also depends on the sex of the child your carrying. My mom swears up and down that she was sick as a dog with my sister and I but was fine with my brother. So go figure.
Not a very strong hypothesis in my opinion. This theory does not answer some basic questions: 1) Why has autism skyrocketed in the last 40 years. 2) Why are some kids perfectly healthy then suddenly become stricken.
It is true that development is affected by the mother. However, you can’t tell me that mothers didn’t have stress or what not before the 1960’s when they weren’t even allowed to vote, have a job, have any rights, and were basically slaves.
Since nobody is commenting on my posts from yesterday or maybe you have not seen my input on how vaccines cause autism, read this:
A highly respected and well-published scientist at the Utah State University, Vijendra K. Singh has further linked autism to the MMR vaccine. His study published in New Foundation of Biology, Elsevier Science BV 2001: 447-58 titled Neuro-immunopathogenesis in Autism provides brain autoantibody and virus serology evidence that links autism to MMR and postulates autism as a neuroautoimmune response that occurs at the neuroimmune biological interface.
Singh found that autoantibodies to myelin basic proteins were present in 80% of autistic children but that none were found in the normal children control group and only rarely in all other controls. These autoantibodies attack the basic proteins that constitute myelin, which surrounds the sheaths of nerve fibers. Regarding the virus serology, autistic children had a significantly higher level of measles virus antibodies as compared to controls, which suggests a temporal link of measles virus with autoimmunity in autism.
Furthermore, Singh found a very important serological association between measles antibody level and antiMBP, which showed that the higher the measles antibody titer the greater the chance of autoantibodies to myelin basic protein. The shocking fact is that none of the children had a wild-type measles infection, but they all had the measles mumps rubella (MMR) vaccine.
Singh also offers hope. He notes an open label trial of oral Sphingolin (myelin containing autoantigen) is being assessed. Preliminary results show significant improvement in autistic people, which further support the neuroimmune pathogenesis in autism.
Vijendra K. Singh, Department of Biology and Biotechnology Center, Utah State University, Logan, Utah, US Researcher links MMR to autism
Then read this piece that explains how auto-antibodies that lead to many different diseases can and are caused by vaccines:
http://liquidzeoliteplus.com/vaccination_dangers.html#genocide
Hence, the whole “mercury causes autism” debate has been a scam to divert attention away from the real cause, the bypass of the natural, evolved path for viruses into the body (lungs) and the barrage of foreign dna, viruses, and “junk” right into the blood steam. Seems to me the drug companies know what they’re doing …..trying to cause disease so that they can come in and treat it (not cure it). Doctors, same thing.
Follow up:
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, Maryland (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 (b) 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@biology.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.latitudes.org/index.html, vol. 4, no. 2, Spring 1999, by Sheila
Rogers: 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)
Very intriguing. I have often pondered a connection between the two disorders, as my grandmother was schizophrenic and my son is on the spectrum and I’ve seen some interesting parallels.
The connection for me began when I read that sensory integration focused OT was effective with schizophrenic patients. Not sure what it all means but it does confirm for me that genetics play a significant role in our neurologic makeup. I’m much more inclined to attribute genetics to my son’s ASD diagnosis than environment because I, too, had none of the risk factors talked about and a “perfect” pregnancy. In fact both of my pregnancies were virtually identical and both resulted in healthy boys except that one is neurotypical and the other is not.
Also, I loved your recent post about what to buy a child who doesn’t really want anything. Our guy’s stocking will be filled with road maps and mini-atlases!
However, he will also get some age-typical gifts like Pokemon cards because in recent years (he’s 9) he has broadened his horizons and is not immune to wanting what his peers have anymore (for better or for worse, it’s hard to say sometimes!).
re: Dr. Singh’s theories. So, autism is the only autoimmune disorder that doesn’t continue to progress? I would think once the myelin was attacked, it would continue to be attacked – if that were the case, all of our children would continue to degenerate, much the same as in Alzheimers, not stabilize and/or improve as time passes.
Has he done any studies later than 1999? Lots has happened in the field since then.
I believe there was some serious refutation of the measles antibody theories in the book Autism’s False Prophets, but I’ll have to go back and look again.
Besides having his work criticized by a panel of drug company lackeys from the UK, nobody has been able to disprove his theories.
Why are his findings thus not well known? No money in this for drug companies. On the contrary. Anything that suggests vaccines may be the cause of disease, if the findings are conclusive and the study well done, is basically ignored in hopes it will be forgotten. I’m here to make sure that doesn’t happen with his work.
This link (http://www.gti.net/truegrit/) from Liquid Zeolite goes to the “Vaccine Injury Coalition,” so I think some of those references need to be read in view of the hypotheses they are assuming.
siliconmom wrote:
yes, that realization has made things better for Charlie in particular and our family—life is short, and why miss a walk in newfallen snow with Charlie scraping his shoes through the slush…..thank you.
Kristina, as you likely know, Science Daily just picks up news releases from universities, etc., and posts them. They’re unvetted by any expert reviewers. This is just a news release publicizing this woman’s dissertation, and frankly, I see little in it that is convincing or even relevant or even new. My favorite part has to be this:
“Ploeger’s research reveals that in the period between 20 and 40 days after fertilisation, the embryo is highly susceptible to disruptions. In this period, early organogenesis, there is a lot of interaction between the different parts of the body. If something goes wrong with a given part of the body, it greatly influences the development of other parts of the body”
Um, duh. Her research most emphatically did not reveal that. Research by thousands of other people long before she showed up revealed that, and it applies to ANY developmental disorder with an etiology based in this time point. I mean, wow.
And then this: “As people with schizophrenia and autism frequently have physical abnormalities to body parts formed during early organogenesis, Ploeger concluded that the foundation for these psychiatric disorders is laid very early during pregnancy.”
The “foundation” may be laid early (in my opinion, the foundation likely forms when the sperm and egg meet), but it’s also laid early for any number of other disorders. That doesn’t mean they’re related, not even remotely so. It’s like saying that because the foundation for being blond or brunet exists at the same timepoint, they both must arise the same way, when in fact, they arise in contrasting ways. And just for the record, it’s my understanding that in autism, at least, the “large head” thing is more related to rapid brain growth postnatally, rather than in utero.
She can “advise” all she wants, but since she appears not to have done an iota of experimental investigation on her own and the entire news release at any rate contains not one thing that is new to developmental biology except for the spurious “correlation,” I’d take that advice and its relevance with about a pound of salt. As Kristina says and I second, we weren’t ancient when we had TH, I was aware of the pregnancy within a week, we were prepared for the pregnancy, and I engaged in no harmful activities, including taking medications or other substances, during any time point in the pregnancy. And as I scan my mind, I cannot think of any other mother of an autistic child whom I know who wasn’t on board in an educated knowledgeable way about pregnancy from the get-go.
This may simply be the world’s worst news release, but if it is even close to an accurate reflection of the findings of this dissertation, I’d just say, “piffle.” And I actually think that dopamine-signaling disorders like schizophrenia are related to autism. I just don’t see the evidence of it cited here. Somebody show me a freaking mechanism already.
TH doesn’t have “protruding ears.”
Frankly, they should have noted this being a summary of her dissertation at the top rather than the bottom——now I am imagining the press release that could have been written about my dissertation……
Liquid… These posts would be better on one of the many vaccine posts. I want to read comments on this topic. Whether u like it or not there is more than one cause to the myriad of asds
I have no issues with a correlative review. Not having seen the dissertation first-hand, it is hard to comment on the actual content, and how much significance to lay on various aspects. I am a little leery of press releases, which often accentuate the least salient points in the primary document.
In the here and now for us, any speculation would be retrospective at best. Focus on today seems more fruitful in the immediate sense.
Happy holidays.
Regan, I’ve got no problem with correlative reviews, either, but whoever wrote this press release certainly didn’t give any information about analysis or real findings from a lit review. I don’t really know how they “do” dissertations in psych, but a “review” wouldn’t cut it in the fields I’m familiar with. It seems to end, rather than to begin, with a hypothesis. Also, this release appears to “quote” her advice. Don’t know if that was direct from the horse or what, but it’s kind of like advising people to brush their teeth every night. Nothing new there. It just seems like there’s nothing new reported from that work while there’s a lot being asserted.
What concerns me is that this has been fed to all the “news” feeds (health, science, etc.) and will probably get picked up as a big headline because of the “woo” factor.
I’ve just done some Googling (yay, Google U) and remain extremely wary of this. I see nothing peer-reviewed from this author published about this. Also, the author is self described as an evo-devo person…but it all seems to be theoretical, rather than empirical, something that also makes me leery. Below is a copy of an abstract from this author from a meeting; I leave you to draw your own conclusions:
“Psychological disorders are common and heritable, but they are also harmful. This leads to an evolutionary puzzle: why did natural selection not eliminate these disorders? Several evolutionary hypotheses have been proposed to explain the origin of disorders such as schizophrenia and depression. I will present a short overview of these explanations, and present an alternative view: the view from evolutionary developmental biology. Evolutionary developmental biologists do not only study the genetic basis of phenotypes, but also how developmental processes influence the phenotype. It is proposed that psychological disorders are not only the result of genetic mutations, but are also due to developmental processes that are easily destabilized. Low robustness of developmental processes is expected when processes are highly interactive and possess low effective modularity. I will present research from an evolutionary developmental perspective that provides evidence for this proposal.”
I could take that abstract sentence by sentence and list several concerns for each. I’m interested in what others think about it.
navi,
Good point, and duly noted. BTW, I never said there was just on cause ….obviously there are a number of factors that need to be in place for damage to occur. I’m more interested in the treatment aspects of this line of study …but I’ll save it for another thread.
Emily,
I agree that quoting “advice” on the basis of this is premature at best, and on googling the Dutch stories, it amounted to–take care of yourself before getting pregnant, which is not exactly breaking news. The “alternative theory” statement is a little bit of a red flag. I agree from what has been put forth that this is in the realm of the theoretical. I’m trying to see if I can locate the full text of this dissertation.
Annemie Ploeger’s webpage
http://home.medewerker.uva.nl/a.ploeger/
Emily, given that this is your area of expertise, I take your opinions as particulary apt.
I did find her home page. I admit to a huge bias–when it comes to dev bio and especially evo devo, I want to see GENES and EMPIRICISM, not theory and correlations. To me, these are things that must be mapped to genetic correlates and molecular pathways, not prematurely publicized with a lot of handwaving. It just makes me edgy to see these things popped out without any mechanistic underpinnings. Also, I am disturbed by apparent gaps revealed in that abstract.
And given the troubled history of schizophrenia and autism, some prudence in reporting about the two together seems more than necessary.
liquid, sorry for the assumption. But it is implied when posted to an unrelated thread. Much like if I pushed genetics on a gfcf post, without commenting on the diet. Thanks. It is good to have an actual citation accompanying a comment like yours though.
Kristina – true. It is also true of the history of mother blaming and autism.
I would like to see more research into relationships with other brain conditions – my husband has bipolar/ ADHD and his mother huntingtons and my self at the very least depression; all of these dxd prior to Tristan’s birth. I also met a caretaker online of an autistic child who’s mother had huntingtons. The chances of meeting, even online, are ridiculously slim …
Huntington’s is a genetic disorder in the way the fragile X is…it’s a trinucleotide expansion disorder in which a triplet repeat of DNA expands in number until it first reaches a threshold called a “premutation,” and then crosses that number threshold so that the person carrying the repeats actually shows symptoms and has a disorder. Usually, with these disorders, the more repeats, the more severe and the earlier the symptoms. If I remember correctly, tuberous sclerosis is also a trinucleotide expansion genetic disorder.
What I mean is this: There will be three nucleotides, e.g, CAG. In people without the disorder, the number of these in a row (CAG-CAG-CAG-CAG) is low. If this number expands–that’s where the “expansion” comes in–to, say, 50 or 100, then you’re on the edge of a problem. If it goes over that threshold, you’ve got a genetic disorder. The expansion occurs with duplications and crossing over events.
I’ve never heard of Huntington’s, which usually has a middle-age onset unless VERY severe, being associated with autism, but certainly TS and Fragile X are.
Yes, I’ve never heard of it, but the odds of having run into another family with both huntington’s and autism, where the autistic child’s autism expressed itself in a way very similar to my son, is so very very very very small, it makes me wonder…
*I* would like to know how many mothers of autistic children drank/used products with aspartame, saccharine, or Splenda….
Ooops, clicked Send…
Really, think about it….obesity epidemic, false arthritis, early breast cancer, thyroid (and hence carb) issues….all these things have been getting worse and worse over the last 40 years.
I think that stuff is one of the culprits.
Ick, can’t stand the stuff. I prefer not sweetened over a substitute
Oh, and thyroid issues are not carb issues… Thyroid issues are caused by lack of iodine frequently.
Never touch that stuff. Ever. Can’t stand it. Gross. I was also caffeine-free during all pregnancies. Organic food. Did all of it. Couldn’t, however, perform any targeted rearrangements of the gene sequences my husband and I bequeathed on the budding little embryos.
FYI, aspartame, Splenda, and saccharine are several “culprits,” not one. And if you’re looking for a cause for breast cancer, there are several far more likely agents.
Thyroid issues are often grounded in T cell misfires that are heritable. Not much to do with carbs.
Let me get this straight: Ploeger’s paper is a review of previous literature, and she’s trying to use the historically abysmally low quality of older research in the mental health fields to guide her to new insights about autism and schizophrenia? Spare me. Cue the gong and the big hook.
LZ: “Besides having his work criticized by a panel of drug company lackeys from the UK, nobody has been able to disprove his theories.”
Um… it’s not for others to disprove his theories; it’s for him to find sufficient evidence to back them up. That’s basically how science works.
Emily: “I don’t really know how they ‘do’ dissertations in psych, but a ‘review’ wouldn’t cut it in the fields I’m familiar with.”
I’m in psychology, and I can tell you that review-based work would not get anyone a Ph. D. in psychology. Not from a reputable university, at least. There would have to be some hypothesis testing. Even in qualitative research.
no artificial sweeteners here……
I keep telling you not to drink the water or give it to your childern that are not at least 10 to 12 years old. As you and they are drinking lead and arsenic which are not good for you when pregant or them at an earily stage of life. When the brain is tell forming!!!
Emily, I say “Culprit” as averse to “culprits” (No Hair Splitting) because they are all Chemical Fake Sugar, which is one Category. There is a documented rise in BC since the use of Aspartame, defending the CFS is just ridiculous. Assuming that any chemical you put into your body (including things like Tylenol) would not potentially harm you or a baby – even before pregnancy – is just naive. All chemicals screw with your molecular makeup.
Navi, in many cases iodine deficiency does seem to be the problem. Although you can’t get doctors to buy it, because that radiation machine and those chemo drugs make money. (You know, the drug company thing again?) Otherwise it would be prescribed for BC and fibrocystic disease.
However, the no-carb craze (or no bread/sugar/white carb craze) represents that the thyroid is the culprit because of carbs. Not iodine. People who have pre-diabetes problems almost always have thyroid issues. Why they only prescribe iodine in the most severe cases is beyond me.
My sincere belief is that this is all – and ONLY – about Money. After the last 8 years, anyone who doesn’t honestly believe that the WHOLE SYSTEM isn’t about Money First is just an ostrich.
Phil Schwarz wrote:
Yes, that’s the case!
They may all be “chemical” fake sugar, but they aren’t all the same chemical, and it’s not hair splitting to say that the body knows that. And your “molecular makeup” is…um, chemical.
I really hate it when people try to sound all sciency without actually knowing any science. That’s not directed at you, Moi, necessarily, but it just drives me nuts because I know that the uneducated person will see something like “chemicals are bad for you!” and just believe it as though it made any kind of sense at all.
You’re gonna have to provide some documentation for what you’re saying about thyroid, carbs, diabetes and thyroid, etc. I’m afraid that you are talking about the link between Type I diabetes and thyroid, which is actually a link forged in the autoimmune nature of both disorders. The highest frequency of the two together occurs among people with type 1 diabetes. The link between thyroid disorder and Type 2 is being elderly…they’re most commonly found together in old people. Given that they’re both intimate participants in the endocrine system, it’s no surprise that the two occur together.
And I have NO IDEA why you’re referencing chemo drugs and a “radiation machine” when discussing thyroid disorders. Are you referring to thyroid cancer, which is treated with RA-I? The body’s I requirement is very low and with iodized salt, I as a factor in thyroid issues in places like the US and where iodized salt is used is rare. The prevalent thyroid disorders are autoimmune disorders involving TPO and other antibodies, not having anything to do with iodine.
Sure, money’s a part of many pursuits. But I can assure you that the people who study the mechanisms of physiology in university labs around the world aren’t doing it for lucre because there ain’t a lot of lucre there.
And Phil…exactly.
If the science was only about $ the last 8 yrs perhaps the administration would not have fought it tooth & nail. And they don’t prescribe iodine for low thyroid that I know of. The salt supplies it. As far as I know they prescribe things like Synthroid. Lack of iodine is not ignored by drs, and the money doesn’t go to big pharmaceuticals (othewise it’d be a pill instead of in salt…) I read about iodine doing a highschool paper in the 90s. I’d hardly call that hidden information…. (I’m not a scientist, was just a kid intersted in a disorder that affected her family members, none of whom have diabetes… Meaning none of the ones with thyroid problems. The ones with diabetes don’t have thyroid problems…)
I have 2 kids on the spectrum and they look normal both have high IQ’s. They’ve actually been asked to model. Some kids with Autism have different DNA than there parents and the same with Schizo. They can do a DNA test to check for some Schizo.
People asked well never used any of that diet crap etc. Didn’t drink, smoke etc. My kids didn’t get MMR on time and still have it. I have no genetic disorder in my family either. Except maybe Asperger’s. Hubby and I under 30 at the time. Normal birth etc.
The only thing I wonder if some how my eggs were injured as a child? I know that found silly but I had a bunch of childhood disease before age 5. I didn’t get completely needled until age 6.
@Amby, thanks for writing about your family—-wondering what you mean by your eggs being “injured”? Are both of your children (if I may ask) pretty much on the same part of the spectrum? Regards—-
Both are on the same part Spectrum. They say some childhood disease can effect reproduction. I wonder if a disease like a virus from childhood can effect unfertilized eggs ?