We might have autism backwards: What “broken mirror” and “broken mentalizing” theories could have wrong - Salon.com »
Yes, these are much better theories.
Yes, these are much better theories.
A goal was to study these parental age effects in more detail by looking at possible differing risks of ASD with and without intellectual disability – one of the most serious comorbid diagnoses with ASD, with a significant impact on functional status in life. This was the first population-based study with an ASD sample large enough to study ASD risk in populations of children with and without intellectual disability.
“When considering risk factors, we can’t necessarily lump all ASD cases together, even though they fall under a broad umbrella of autism,” Lee said. “We need to keep an open mind in case intellectual disability might be a marker of a different underlying mechanism.”
The finding that ASD with intellectual disability had a stronger association with older parents, compared to ASD without intellectual disability, supports continued investigation of possible different mechanisms.
There. Fixed it.
Image descriptions: Image #1: Black text on white background reading “CURE AUTISM” with the word autism covered over by a green label reading “ABLEISM”. Image #2: Black text on white background reading “PREVENT AUTISM” with the word autism covered over by a brown label reading “HATRED”. Image #3: Black text on white background reading “COMBAT AUTISM” with the word autism covered over by a yellow label reading “STIGMA”. Image #4: Black text on white background reading “FIGHT AUTISM” with the word autism covered over by a red label reading “IGNORANCE”.
UC San Diego researchers have found clear and direct new evidence that autism begins during pregnancy, reporting that patches of disrupted brain development occur in the womb.
Researchers at the University of California, San Diego School of Medicine and the Allen Institute for Brain Science have published a study that gives clear and direct new evidence that autism begins during pregnancy.
The study will be published in the March 27 online edition of the New England Journal of Medicine.
The researchers – Eric Courchesne, PhD, professor of neurosciences and director of the Autism Center of Excellence at UC San Diego, Ed S. Lein, PhD, of the Allen Institute for Brain Science in Seattle, and first author Rich Stoner, PhD, of the UC San Diego Autism Center of Excellence – analyzed 25 genes in post-mortem brain tissue of children with and without autism. These included genes that serve as biomarkers for brain cell types in different layers of the cortex, genes implicated in autism and several control genes.
“Building a baby’s brain during pregnancy involves creating a cortex that contains six layers,” Courchesne said. “We discovered focal patches of disrupted development of these cortical layers in the majority of children with autism.” Stoner created the first three-dimensional model visualizing brain locations where patches of cortex had failed to develop the normal cell-layering pattern.
“The most surprising finding was the similar early developmental pathology across nearly all of the autistic brains, especially given the diversity of symptoms in patients with autism, as well as the extremely complex genetics behind the disorder,” explained Lein.
During early brain development, each cortical layer develops its own specific types of brain cells, each with specific patterns of brain connectivity that perform unique and important roles in processing information. As a brain cell develops into a specific type in a specific layer with specific connections, it acquires a distinct genetic signature or “marker” that can be observed.
The study found that in the brains of children with autism, key genetic markers were absent in brain cells in multiple layers. “This defect,” Courchesne said, “indicates that the crucial early developmental step of creating six distinct layers with specific types of brain cells – something that begins in prenatal life – had been disrupted.”
Equally important, said the scientists, these early developmental defects were present in focal patches of cortex, suggesting the defect is not uniform throughout the cortex. The brain regions most affected by focal patches of absent gene markers were the frontal and the temporal cortex, possibly illuminating why different functional systems are impacted across individuals with the disorder.
The frontal cortex is associated with higher-order brain function, such as complex communication and comprehension of social cues. The temporal cortex is associated with language. The disruptions of frontal and temporal cortical layers seen in the study may underlie symptoms most often displayed in autistic spectrum disorders. The visual cortex – an area of the brain associated with perception that tends to be spared in autism – displayed no abnormalities.
“The fact that we were able to find these patches is remarkable, given that the cortex is roughly the size of the surface of a basketball, and we only examined pieces of tissue the size of a pencil eraser,” said Lein. “This suggests that these abnormalities are quite pervasive across the surface of the cortex.”
Data collected for the Allen Brain Atlas, as well as the BrainSpan Atlas of the Developing Human Brain was developed by a consortium of partners and funded by the National Institute of Mental Health. It allowed scientists to identify specific genes in the developing human brain that could be used as biomarkers for the different layer cell types.
Researching the origins of autism is challenging because it typically relies upon studying adult brains and attempting to extrapolate backwards. “In this case,” Lein noted, “we were able to study autistic and control cases at a young age, giving us a unique insight into how autism presents in the developing brain.”
“The finding that these defects occur in patches rather than across the entirety of cortex gives hope as well as insight about the nature of autism,” added Courchesne.
According to the scientists, such patchy defects, as opposed to uniform cortical pathology, may help explain why many toddlers with autism show clinical improvement with early treatment and over time. The findings support the idea that in children with autism the brain can sometimes rewire connections to circumvent early focal defects, raising hope that understanding these patches may eventually open new avenues to explore how that improvement occurs.
What I wish would happen as the result of autism research: Better and more focused treatment options and services for autistic people like me.
What will probably happen instead: increased pressure on people to have eugenic abortions.
Additionally, before anyone jumps in with the wrongheaded idea that I’m again abortions for anyone who needs one: no. I’m against stigma, ableism, misinformation, and the total lack of informed consent and abuses that go on in the medical community when prenatal testing for any disability becomes available, as has occurred with Down Syndrome:
womenare unprepared to make prenatal decisions about fetuses diagnosed with Down Syndrome because of societal pressures to have “normal” children, a negative view of persons with disabilities by many in society, a fear of legal liability by those in the medical community, the lack of genuine informed consent before undergoing genetic testing and abortion, and the failure of non-directive pre-abortion counseling in the medical community.
Moreover, medical professionals fail to communicate correct and unbiased information before and during the genetic screening, diagnostic testing, and abortion decision-making process. This article addresses the contributing factors and causes that ultimately lead to a lack of informed consent and a very high abortion rate for fetuses diagnosed with Down Syndrome.
I’m not against increasing our knowledge; it’s the LACK of information I’m against. I think information like this will be used to try and prevent autistic people from existing instead of trying to help autistic people who are alive right now, and heavily stigmatized, abused, and murdered because we’re autistic.
This is huge news. I really hope this puts the cause of autism debate to rest and we can move on to using all the money researching that to supporting families and adults with autism. Supports are desperately needed.
everything in the world that might help me is geared towards children
Casual reminder that Donald T., the first person ever diagnosed with autism in this country, sang in his school choir, graduated from high school, earned a college degree in French, drives, golfs, travels for fun, has a circle of friends, and lives on his own.
This is the person with, literally, the prototypical case of autism.
So if you’re making an argument that any given person is too “high-functioning” for their input to count in the national discussion about autism, or that Autism Speaks is “not really talking about people like you,” when they call autism a national catastrophe, when they call us lost, missing, kidnapped, diseased, burdens on our families and society, and lobby for our elimination…you may need to recalibrate your ideas about autistic people a little bit.
Autism Speaks’ only advisory board member on the autism spectrum, John Elder Robison, announced his resignation from the organization this month in protest of the organization comparing autistic people to kidnapping victims and claiming that our families are not living, but merely existing, due to the horror of having autistic people in their lives. In his resignation letter, he discusses his four years spent attempting to reform the organization from the inside without success, stating, “Autism Speaks says it’s the advocacy group for people with autism and their families. It’s not, despite having had many chances to become that voice. Autism Speaks is the only major medical or mental health nonprofit whose legitimacy is constantly challenged by a large percentage of the people affected by the condition they target.”
“If you truly want to spread autism awareness, why do 95% of all autism organizations only or predominately mention only children?”
SOMETHING WAS WRONG with Kai Markram. At five days old, he seemed like an unusually alert baby, picking his head up and …
Interesting read. I’m only halfway through it, but I wanted to share it with everyone.
I agree with much of this. This is my experience of the world - intense, powerful, overwhelming.
Good. This is good.
…One thing that seems to have gone unvisited in any of these studies is the question of which might come first: Autism, or wheat sensitivity?
The current consensus is that a “leaky gut” on its own isn’t sufficient to cause disease, and what remains unknown is if an existing disorder causes a leaky gut–produces gaps in the intestinal barrier that’s supposed to be largely impermeable–or if a leaky gut eventually leads to a disorder. Because studies have yet to show that repair of a “leaky gut” is effective treatment for anything, some authors have suggested that rather than focusing on the gut for therapy, the focus should be on the primary cause underlying the leaky gut. In the case of autism, which is typically associated with high levels of anxiety and stress, could stress and anxiety be the cause of increased gut permeability?
Stress is sufficiently linked to gut permeability that a rat model of this problem uses stress to trigger the leaky gut in the animals. Restraint and acoustic stress induced in mice is linked to neuroinflammation and gut permeability. In other words, to quote one abstract, “stress induces increased permeability of the gut.” Indeed, studies indicate that stress can, in fact, lead to “food antigen-related adverse responses” (i.e., antibody attack of proteins ingested in food), in addition to increased intestinal permeability. Could autistic people, who tend to experience high anxiety and stress, be more prone to a leaky gut, allowing wheat proteins to slip past the barrier and trigger the antibody response?The stress in question here is not “toxins” or metabolic or oxidative stress. It’s stress from anxiety, restraint, emotional distress, and acoustic torture. Is it possible that thanks to a certain paper alleging a link between vaccines and gut, published back in 1998 and later retracted, the research community has since been looking at the gut-autism connection from the wrong vantage point? Perhaps it’s not that gut leakage causes autism, but that the anxiety of autism stresses the gut…
Sense, this makes.
Dyspraxia has been, for the most part, renamed Developmental Coordination Disorder (DCD).
From Medical News Today:
A person with dyspraxia has problems with movement, coordination, judgment, processing, memory and some other cognitive skills. Dyspraxia also affects the body’s immune and nervous systems.
Dyspraxia is also known as Motor Learning Difficulties, Perceptuo-Motor Dysfunction, and Developmental Coordination Disorder (DCD). The terms Minimal Brain Damage and Clumsy Child Syndrome are no longer used.
Developmental coordination disorder (DCD) also known as developmental dyspraxia and “clumsy child syndrome” is a chronic neurological disorder beginning in childhood that can affect planning of movements and co-ordination as a result of brain messages not being accurately transmitted to the body. Up to 50% of dyspraxics have ADHD. It may be diagnosed in the absence of other motor or sensory impairments like cerebral palsy, muscular dystrophy, multiple sclerosis or Parkinson’s disease.
People with developmental coordination disorder sometimes have difficulty moderating the amount of sensory information that their body is constantly sending them, so as a result these people are prone to panic attacks. Having other autistic traits (which is common with developmental coordination disorder and related conditions) may also contribute to sensory-induced panic attacks.
To put it simply, it’s the brain’s inability to plan muscle movements and carry them out. What you think you want to do is not always what happens. Sometimes there is success in an action, sometimes it’s a complete clumsy failure. It also has a lot to do with the processing of sensory information, leading to a great deal of oversimulation from external sources. Dyspraxia can range from verbal to mental to physical. It can affect the ability to understand language, read social cues, recognize danger, and speaking. It can limit motor skills and physical coordination.
With Autism Spectrum and Dyspraxia, there is often some overlap. In my experience, coordination was never great. It makes it hard for me to do as well as my friends at games that require a lot of it (Like Beatmania and Dance Dance Revolution, though I won’t say I suck at them). If I don’t practice a lot, I quickly lose the skills I’ve gained. I do NOT do aerobics classes because of it. Of course, let’s not forget social awkwardness around the average NT crowd; I hang out with geeks and other Aspies for a reason. (MY PEOPLE.)
Autism.org.uk has some GREAT information on Dyspraxia and how it relates to autism. It’s a good read!
I don’t care how well known or famous you are in the field of autism, if you are not engaged in reading and talking to Autistic people outside of a clinical setting, you have more to learn.
If you’ve been taught a particular therapy or teaching method is the only scientifically proven method to “treat” or teach Autistic children, find Autistic people who were given that therapy or method as children and learn what they have to say about it. If you find a number of Autistic people are speaking out about a specific treatment or method, saying they have post traumatic stress as a direct result, reconsider your position. If you still feel this therapy is important to pursue, ask yourself why and at the very least, inform the parents who are considering this method that there are Autistic people who believe it was damaging to them. It doesn’t matter whether non autistic people and professionals agree, you have an ethical obligation to tell parents that this treatment or method has caused damage to a great many.