“First off, Autism Speaks is an anti-autistic hate group. Don’t use them for a source. In fact, if you paid any attention AT ALL to neurodiversity proponents, they DO advocate pathologizing and treating the co-morbid conditions. That doesn’t mean we want to change the way we think. Autism is part of who we are. We shouldn’t “treat” autism, but we should treat Autistics for the same things we treat non-autistic people, such as diseases like epilepsy. “
The “Autism Speaks” link I used was merely for the economic statistics, which still stand on their own regardless of who reports them. I am not claiming to agree with everything this organization does nor was that my point. Now, moving on to your other claims—I am specifically addressing those within the neurodiversity who do trivialize and downplay the co-morbidities. I did not claim that every single person within this movement was wrong or that all of their viewpoints were incorrect; I outlined the signature arguments and assumptions that were flawed. I myself have debated those who deny that their is an association between autism and co-occurring morbidities, which is another reason I have pointed this out. In fact, I said “To be clear, I am not claiming that autistic people shouldn’t be accepted or looked at equally; they should be loved, appreciated, and regarded with compassion and empathy.” The problem arises when there is ignorance of the negative effects of the autism epidemic and what a statistically significant portion of autistic people go through. I am also not claiming that every idea the neurodiversity movement has put forth is wrong; I am only showing the part of it that is demonstrably false and entirely ignorant of reality. Mainly, looking away from these valid findings and data on autism is both asinine and counterproductive.” To reiterate my point once more, autism is biological. Specific subgroups within autism have the behavioral abnormalities they do due to underlying disease and occurrences such as brain inflammation, oxidative stress, immune abnormalities, and mitochondrial dysfunction. These are medically treatable in specific cases and they are related to the behavioral phenotype. You say you don’t want to change the way “we” think, but you need to realize you do not speak for every single person with autism. When you say “we” you are speaking of yourself and the others within the ND movement, but this does not include all of them; I find this important to note when discussing differences in ideas and perceptions.
“Autism is also not an epidemic. We have always existed. And most of the evidence claiming environmental causes is questionable at best.”
The contention that “autism is not an epidemic” is false. The statistics and science say otherwise:
Nevison, C. (2014). a comparison of temporal trends in United States autism prevalence to trends in suspected environmental factors. Environ Health, 13(73). Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177682/
“The quantitative comparison of IDEA snapshot and constant-age tracking trend slopes suggests that ~75-80% of the tracked increase in autism since 1988 is due to an actual increase in the disorder rather than to changing diagnostic criteria.”
Dave, D., Fernandez, J. (2014). Rising autism prevalence: Real or displacing other mental disorders? Evidence from demand for auxiliary healthcare workers in California. Economic Inquiry. Retrieved from http://onlinelibrary.wiley.com/doi/10.1111/ecin.12137/abstract;jsessionid=EDA31CC40A2BC6358D480853F07EC7BC.f01t01
These estimates suggest that at least part of the increase in autism diagnoses, about 50–65%, reflects an increase in the true prevalence of the disorder. (JEL L11, J2, J3)
DeSoto et al. (2013). Professional opinion on the question of changes in autism incidence. Open Journal of Psychiatry. Retrieved from http://www.scirp.org/Journal/PaperInformation.aspx?paperID=30182
Results suggest that among professional psychologists with a terminal degree (n=88), the majority believe that diagnostic changes can not fully account for the observed increase; 72% reported wither the true rate may have, or definitely has, increased
Hertz-Picciotto et al. (2009).UC Davis M.I.N.D. Institute study shows California’s autism increase not due to better counting, diagnosis. UCDavis Health System. Retrieved from http://www.ucdmc.ucdavis.edu/welcome/features/20090218_autism_environment/
Published in the January 2009 issue of the journal Epidemiology, results from the study also suggest that research should shift from genetics to the host of chemicals and infectious microbes in the environment that are likely at the root of changes in the neurodevelopment of California’s children.
I am also not claiming that autistic people have not always been around; they have, but the prevalence and rates were not as high. We now know that a specific percentage of the observed increase is due to actual increases in autism and not just diagnostic changes.
Your statement that the evidence of environmental causes is “questionable at best” is also an assumption and an opinion, albeit not a scientific one. There are known environmental contributions to autism and there are potential causes which are continuing to be studied. Here are some (a small number out of the many existing) scientific citations:
We estimated how much of the probability of developing ASD can be related to genetic (additive and dominant) and environmental (shared and nonshared) factors… Heritability of ASD and autistic disorder were estimated to be approximately 50%. These findings may inform the counseling of families with affected children.
Children of mothers who live near agricultural areas, or who are otherwise exposed to organophosphate, pyrethroid, or carbamate pesticides during gestation may be at increased risk for neurodevelopmental disorders. Further research on gene-by-environment interactions may reveal vulnerable sub-populations.
This work builds upon the theory that ASDs are a spectrum of disorders with prenatal origins, where both genetic and environmental factors contribute to atypical neurodevelopment, resulting in more autistic behaviors, and, at the extreme end, clinical diagnosis. EDCs deserve consideration as candidate risk factors for ASDs because of their potential to alter hormonal axis functions that play an important role in neurodevelopment. Building on this, we employed a statistically rigorous design to screen 52 different candidate EDCs and identify those worth additional study
Disease clusters are defined as geographically compact areas where a particular disease, such as a cancer, shows a significantly increased rate. It is presently unclear how common such clusters are for neurodevelopmental maladies, such as autism spectrum disorders (ASD) and intellectual disability (ID). In this study, examining data for one third of the whole US population, the authors show that (1) ASD and ID display strong clustering across US counties; (2) counties with high ASD rates also appear to have high ID rates, and (3) the spatial variation of both phenotypes appears to be driven by environmental, and, to a lesser extent, economic incentives at the state level.
Rossignol et al. (2014). Environmental toxicants and autism spectrum disorders a systematic review. Translational Psychiatry. Retrieved from http://www.nature.com/tp/journal/v4/n2/full/tp20144a.html#bib13
2. ASD is presenting as a systemic abnormality creating immune dysregulation/inflammation, impaired detoxification, redox regulation/oxidative stress, and mitochondrial dysfunction. Caused by toxicant exposures with genetic interplay.
The findings of this review suggest that the etiology of ASD may involve, at least in a subset of children, complex interactions between genetic factors and certain environmental toxicants that may act synergistically or in parallel during critical periods of neurodevelopment, in a manner that increases the likelihood of developing ASD. Because of the limitations of many of the reviewed studies, additional high-quality epidemiological studies concerning environmental toxicants and ASD are warranted to confirm and clarify many of these findings.
The researchers warn that chemical safety checks need to be tightened up around the world to protect our vulnerable youngsters from a ‘silent epidemic’ of brain disorders.
These findings suggest that infantile zinc- and magnesium-deficiency and/or toxic metal burdens may be critical and induce epigenetic alterations in the genes and genetic regulation mechanisms of neurodevelopment in the autistic children, and demonstrate that a time factor “infantile window” is also critical for neurodevelopment and probably for therapy. Thus, early metallomics analysis may lead to early screening/estimation and treatment/prevention for the autistic neurodevelopment disorders.
It is a multifactorial disorder resulting from interactions between genetic, environmental and immunological factors. Excitotoxicity and oxidative stress are potential mechanisms, which are likely to serve as a converging point to these risk factors. Substantial evidence suggests that excitotoxicity, oxidative stress and impaired mitochondrial function are the leading cause of neuronal dysfunction in autistic patients. Glutamate is the primary excitatory neurotransmitter produced in the CNS, and overactivity of glutamate and its receptors leads to excitotoxicity. The over excitatory action of glutamate, and the glutamatergic receptors NMDA and AMPA, leads to activation of enzymes that damage cellular structure, membrane permeability and electrochemical gradients. The role of excitotoxicity and the mechanism behind its action in autistic subjects is delineated in this review.
Autism spectrum disorders (ASDs) are caused by both genetic and environmental factors. Mitochondria act to connect genes and environment by regulating gene-encoded metabolic networks according to changes in the chemistry of the cell and its environment. Mitochondrial ATP and other metabolites are mitokines—signaling molecules made in mitochondria—that undergo regulated release from cells to communicate cellular health and danger to neighboring cells via purinergic signaling
Here you are attacking a straw man, using false equivalence, avoiding the issue, and using an appeal to emotion. The cost to to the economy is a fact and it is not implying that they are “burdens.” It is looking at the reality of financial costs for autistic people and their families and how this affects the economy along with overall life.
“In 2011, Autism Speaks awarded Dr. Leigh’s a research grant to develop clear and reliable methods to update autism’s economic costs to society on an annual basis. Such information is crucial when advocating for support services that reduce overall costs to society while improving daily function and quality of life.
In his work, Dr. Leigh included analysis of both direct and indirect costs.
Direct costs include special education, adult care programs, physician and therapist visits, hospitalizations, medications and paid caregivers.
Indirect costs include lost productivity – particularly in terms of wages and benefits – for both those who have autism and their family caregivers.
Information for the analysis came from the Centers of Disease Control and Prevention, the Bureau of Labor Statistics and published research estimates of per-person costs.
“Public, research and government policy attention to autism ought to be at least as great as it is for other major health conditions such as diabetes,” concludes Dr. Leigh.”
The data and information is being used to assess the reality of costs and also improve the lives of those with autism, not to “reduce us to nothing more than financial burdens.”
As for your statement about nazis and Aktion T4, I am not advocating for euthanasia nor is any of this related to the arguments I put forth about autism. I am not “basically saying that we don’t deserve to exist/our lives aren’t worth living just because we’re an inconvenience.” The logical fallacy your using is a straw man.
Your nescience seemingly undermines your ability to understand how brain inflammation affects cognitive function and how this translates into specific autistic phenotypes. Although I am interested in open dialogue about autism, science, and the implications of our current state of knowledge, I highly doubt (with you) that this will blossom into a productive, open, and interesting philosophical debate.