I thought I would share the main points here.
Link to paper 👇
CBT has not yet been shown to be effective for autism.
There is no empirical support yet for early intervention.
Evidence for Aspergers as a separate disorder is very weak.
Social skills training appears not to translate to real-world social skills.
Hertitabity doesn’t tell us about individuals, but we know that if a newborn infant has a first-degree relative with autism, there is a 20% chance they will be autistic too.
ADHD drugs DO work and are tolerated well in MOST people with co-occurring ADHD.
Oxytocin and vasopressin studies are underpowered and show mixed results which are not promising.
Indeed autism lowers the quality of life of the whole family more than any other neurodevelomental condition.
And I quote now -
“Terms such as “disease” are inappropriate and are scientifically inaccurate when referring to autism”
Pity nobody told the tutors @KingsCollegeLon
Objective measures use independence and ability to work as main markers.
Women with autism have a harder time maintaining employment than men- it is not yet clear why.
Do not go to your naturopath for help with your autistic child, you risk harming them.
Focus playtime intervention has been shown to be ineffective.
Preschool Autism Communication Trial (PACT) did not alter core autism traits.
Early Start Denver Model - there is some evidence of mild reductions in autism traits but evidence is mixed.
When an adult goes for a diagnosis we are still using tools made for diagnosing children.
Rectifying this was identified as an URGENT need.
The heterogeneous nature of autism is further complicating interpretation of results.
Autistic people do not have a broken brain mirror.
We don’t yet know why the evidence is so mixed but it is likely due to the heterogeneous nature of autism.
No MRI results are definitive.
Neonatal hypoxia, gestational diabetes, <12 month pregnancy interval, maternal age >40, paternal age >50, older autistic sibling, preterm birth, maternal obesity, folic acid deficiency, valproate use during pregnancy.
Premature rupture of membranes, hypertension in pregnancy, prenatal smoking, c-section, assisted vaginal delivery, IVF, prolonged labour, vaccination.
Prenatal exposure to pesticides, family history of auto-immune disorders, summer birth, air pollution exposure.
Such research has told us very little about the pathophysiology of autism.
Animal models cannot inform us as to complex human social disability.
“Addressing a single autism mutation at a time is not synonymous with an easy avenue to clinical care of most people with autism”.
Inc. TOM, social motivation theory, weak central coherence, enhanced perceptual processing, executive function deficits, attentional control deficits etc.
“The consensus on the potential explanatory value of these theories have declined in the past decade”
Male brain; TOM; infant social orienting deficit etc.
“Lack specificity, are largely non-developmental, applying only to a single point in time, and lack evidence as explanatory models.”
Next major area for investigation- how do these same gene mutations lead to diverse phenotypes?
This is in line with what autistic people have been saying about their experience.
The genes seem to be involved in chromatin remodeling, synapse formation and synaptic functioning.
diverse autism genetics may contribute to final common pathways of functional difference.
Autism won’t likely be a “thing” in the biological/medical/research world in a few years time.
Community priories are “strikingly seldom prioritied in autism research”
“To move from science to practice, including evaluation and treatment, autism researchers need to find a way to select and fund studies of more mundane, but critical evidence gaps in understanding”
i.e stop measuring mouse-vocalisations and arse-sniffing and focus on measurable biology.
These views are not mine.
That said, this was the best scientific paper I have read on autism.
As well, they use the term “sensory-anomalies” instead of “sensory-deficits/disorders” 👍
Beware of twin studies.
Infants who develop autism actually have normal profiles regarding interest in faces and eyes at 6months of age casting doubt on social orientation theories of autism.
Rather, complex bi-directional developmental interactions between environment/genes/synaptic signalling etc. likely produce diverse autism phenotypes.
Most animal studies don’t address the genetics of most autistic people AT ALL.
Such therapies are supported more in the US than in other countries where they are more controversial.
Some more impacted autistics in a sample drags average down.
Published results make it seem like ALL autistic people can’t perform a task when in fact many CAN and some will perform it to a superior level.
fMRI researchers in particular... take note!!!
We must stop pooling heterogeneous populations into single studies.
What this means, and how we might treat it - if indeed that’s what is desired - we as yet do not know.
Relying on clinical opinion is not enough. We need proper methods to help clinicians accurately differentiate.
Some studies show autistic people more likely to be diagnosed with other health conditions such as immune, sleep disorders, obesity.
Yet some groups within the autistic population may not in fact have reduced lifespan at all
“This theory has not yet been empirically supported”
“The distance between science and practice remains great, and the amount of research that attempts to address solvable problems for autistic people alive today and their families remains modest”
Thanks for listening all!