Poistettu Aamupaskan blogeista.
Kerrakin oli hyvä YLE1:n PRISMA, ja vieläpä psykiatrian kuumimmasta perunasta autismista ja lopultakin yhä tuntemattomista syistä ja mekanismeista!
Erinomainen ohjelma kerrankin.Jokohan se tähän lopultakin loppui:YLE:n ja Suomen valtion joukkomurhaan rinnastettava "peilineuroni"autismiuoskarointi!? En väitä, että autismi olisi yksinomaan suolistobakteerien tuottamien kemikaalien syytä, mutta mitään "peilineuroneita" EI YLIPÄÄTÄÄN OLE LAINKAAN OLEMASSA. Kyseessä on ollut tietoinen ja harkittu lääketieteen väärentäminen ((tyhmyyttään) oletetuista) "poliittisista syistä".
(Minkähän tason nootti tuohon on Jenkeistä /Kanadasta /Britanniasta/ WHO:lta tarvittu ...)
" Uutiset Radio ja TV
DOKUMENTTI
Löytyykö apu ruokavaliosta
Dokumentti esittää uusia näkökulmia autismiin ja sen tutkimukseen 22.7.2013 2:00
Prisma: Autismin arvoitus
The Autism Enigma, USA 2011
Ohjaus Marion Gruner
TV1 klo 19.00
Dokumentti alkaa mieleenpainuvilla faktoilla. Sen mukaan autismi on Yhdysvalloissa ja Ruotsissa neljä kertaa yleisempää somaliyhteisöissä kuin muissa ryhmissä, ja oireyhtymä on lisääntynyt dramaattisesti myös valtaväestön keskuudessa.
Biokemian professori Jeremy Nicholson uskoo, että 30 vuoden kuluttua eriasteiset autismin oireet ovat pikemmin- kin "sääntö kuin poikkeus" pohjoisamerikkalaisten keskuudessa. Mitä oikein on tapahtunut? Miksi autismi yleistyy niin nopeasti?
Tutkijoilla ei ole yksiselitteistä vastausta, mutta jotkut asiaan perehtyneet uskovat, että syy saattaa löytyä suolisto- bakteereista.
Länsi-Ontarion yliopiston neurotutkija Derrick MacFabe on vakuuttunut asiasta. Monilla autistisilla lapsilla esiintyy ruoansulatusoireita, ja MacFaben mukaan ruoan-sulatuselimistön ongelmat voivat johtaa autismin puhkeamiseen tai pahenemiseen.
MacFabe esittää näkemyksiään Chicagossa järjestettävässä autismikonferenssissa, jossa kuulijoina on tutkijoita ja autistien läheisiä eli ihmisiä, joilla on taustatietoa aiheesta.
Tavalliselle tv-katsojalle dokumentin lääketieteelliset faktat ja teoriat ovat välillä haastavia, ja niiden ymmärtäminen vaatii herpaantumatonta keskittymistä.
Dokumentin tekijät ovat kuitenkin tiedostaneet tilanteen. He avaavat asiantuntijoiden puheita konkreettisilla esimerkeillä, joiden kautta katsoja hahmottaa paremmin näkemäänsä.
Heti alussa tavataan somalitaustainen, Kanadassa asuva Adar Hassan, jonka nel-jästä lapsesta kahdella on autismi. Hassanin kokemukset tukevat MacFaben teoriaa: hänen poikiensa Alin ja Abshirin autismin oireet helpottivat, kun vatsaongelmat loppuivat. Lasten keskittymiskyky parani ja levottomuus väheni, kun Hassan muutti lastensa ruokavaliota ja alkoi valmistaa ruokaa tuoreista raaka-aineista.
Ruokavalio saattaa selittää myös sen, miksi autismi on yleistä erityisesti afrikkalaisten maahanmuuttajien keskuudessa.
Lontoon Imperial Collegen biokemian professorin Jeremy Nicholsonin mukaan autismia on eniten teollistuneissa maissa. Hän uskoo, että syy löytyy prosessoidusta ruoasta ja antibioottien käytöstä elintarviketeollisuudessa. Nicholson pitää loogisena sitä, että Afrikasta Kanadaan muuttaneet somalialaiset sairastavat länsimaalaisten tauteja, koska heidän elintapansa ovat muuttuneet länsimaisiksi.
Erityisen mieleenpainuvaa dokumentissa on yhdysvaltalaisen Ellen Bolten ja hänen autistisen Andy -poikansa tarina. Bolte ei ole lääketieteen ammattilainen, mutta hän alkoi omin päin tutkia poikansa autismia.
Bolte kehitteli teorian, jonka mukaan Andyn korvatulehdukseen syömä antibiootti on vaikuttanut suolistobakteerei- hin ja lopulta aiheuttanut autismin. Hoidoksi Andy sai lääkäriltä voimakkaan vankomysiiniantibioottikuurin, joka lievensi oireita, mutta vain tilapäisesti. Kuurin jälkeen Andyn autismi palasi ennalleen, eikä vankomysiiniä voi syödä jatkuvasti.
Bolte on kuvannut kotivideokameralla Andyä ennen kuuria ja sen aikana. Muutamas-sa viikossa tapahtunut muutos on dramaattinen: sulkeutunut ja silmin nähden sairas lapsi alkoi leikkiä ja liikkua normaalisti.
Vanhat kotivideot tekevät vaikutuksen.Ne näyttäytyvät katsojalle todisteena siitä, että lääkäreiden teoria suolistobakteereiden ja autismin yhteyksistä voi pitää paikkansa. Autismin arvoitus on monimutkainen dokumentti monimutkaisesta aiheesta, mutta silti hyvin avartava.
Moni asiaan vihkiytymätön varmasti uskoo, että autismi on pysyvä aivojen ke-hityshäiriö.Dokumentin mukaan tämä ajatusmalli on ainakin osin vanhentunut. "
Ei ole mikään ihme,että on väärinkäsityksiä,kun Suomenkin koko (terroristi)media on yhdenmukaistetusti jauhanut tuota toista, väärää "vaihtoehtoa" yli 10 vuotta, lopulta-kin vain yhden antifasistilehden, Kansan äänen, ja ulkomaisen tiedelehdistön, erityisesti Scientific Americanin sekä tietysti netin rikkoessa "rintamaa"...
Teorian ympäristökemikaalaista erityisesti joissakin asutuskeskuksissa jo 50-luvun NL:ssakin yleistyneen autis- min (eräinä) syinä esitti ensimmäisenä eläkepäivillään akateemikko, Ivan Pavlovin assistentti ja instrumentaalisten ehdollisten refleksien olemassaolon toteennäyttäjä (1927, samana vuonna kuin Pavlovim perusteos) Anatoli Georgijevitsh Ivanov-Smolenski.
https://wrongplanet.net/forums/viewtopic.php?t=231327
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https://scitechdaily.com/using-blood-to-uncover-the-secrets-of-one-type-of-autism/
" Using Blood To Uncover the Secrets of One Type of Autism
Research from the UC Davis MIND Institute sheds light on maternal autoantibody-related autism
A neurodevelopmental condition called autism spectrum disorder affects 1 in 44 kids in the United States. It has a broad range of characteristics with various intensities and origins. Maternal autoantibody-related autism spectrum disorder (MAR ASD) is one kind of autism.
The presence of certain maternal immune proteins known as autoantibodies that respond to certain proteins identified in the fetal brain characterizes MAR ASD. Ma-ternal autoantibodies (IgG) pass the placenta and enter the developing brain. Once there, they may alter the way the brain develops in children, resulting in autism-like symptoms.
Two new UC Davis MIND Institute studies are helping us learn more about this kind of autism. They discovered evidence for predictive protein patterns in the blood of pregnant women, as well as correlations between MAR ASD and greater intensities of autistic symptoms.
MAR ASD patterns linked to autism before birth
The MIND Institute’s Judy Van de Water and a team of researchers showed that autoantibody binding to nine specific combinations of proteins (known as MAR ASD patterns) successfully predicts autism in previously diagnosed children. They tested maternal blood samples collected during pregnancy to see if they could validate the identified patterns. They wanted to see if the patterns accurately predicted autism in the children. Their study findings were recently published in the journal Molecular Psychiatry.
Judy Van de Water, UC Davis professor of immunology and neurodevelopment, and senior author of the study.
“Previously,we identified nine patterns linked to MAR ASD.In this study,we wanted to check the accuracy of these patterns in predicting MAR ASD. To do that, we tested plasma from pregnant mothers, collected by the Early Markers for Autism (EMA) study,” said Van de Water, the study’s senior author. Van de Water is a UC Davis professor of immunology and neurodevelopment.
The study screened the plasma of 540 mothers of autistic children, 184 mothers of kids with intellectual disability but no autism, and 420 general population mothers of kids with no known autism or intellectual disability at the time of the study.
It found reactivity to at least one of the nine MAR ASD patterns in 10% of the autistic group.This is compared with 4% of the intellectual disability group for some patterns, and 1% of the general population group. Four patterns were present only in mothers whose children were later diagnosed with autism, making those particular autoantibody patterns highly predictive.
The study also found that a mother with reactivity to any one of the nine MAR ASD patterns has around 8 times the chance of having an autistic child.
Several MAR ASD patterns were strongly associated with autism with intellectual disability. Others were linked to autism without intellectual disability. The protein pat-tern most strongly linked to autism was (CRMP1+CRMP2).It increased the likelihood of an autism diagnosis by 16 times and was not found in the non-autism groups.
MAR ASD similarly present across states
Previous research found the MAR subtype of autism in 20% of a Northern California sample of autistic kids Yet, until now, this type of autism has not been studied in any state besides California.
A team of researchers led by Kathleen Angkustsiri explored MAR ASD in two new clinical sites:the Children’s Hospital of Philadelphia (CHOP) and Arkansas Children’s Hospital and Research Institute (ACHRI). Their study, published in The Journal of Developmental and Behavioral Pediatrics, recruited 68 mothers of autistic children ages 2-12 years. The mothers provided blood samples and completed behavioral questionnaires about their children.
Early diagnosis allows for customized child support. Credit: University of California – Davis Health
The study also included data from the children’s clinical diagnostic assessments. It used established diagnostic measures known as ADOS (the autism diagnostic observation schedule) and Social Communication Questionnaire (SCQ) to assess the children’s autistic characteristics.
MAR ASD was present in 21% of CHOP’s and 26% of ACHRI’s samples. Overall, 23.5% of the blood samples were considered MAR positive (+MAR), showing autoantibodies reacting to known MAR ASD protein patterns.
“Our study showed similar MAR ASD frequencies in two other states similar to what we observed in Northern California,” Angkustsiri said. Angkustsiri is an associate professor of developmental-behavioral pediatrics at UC Davis Children’s Hospital and the UC Davis MIND Institute and the study’s lead author. “This suggests that the prevalence of MAR ASD is consistent across different demographics and geographic settings.”
MAR ASD and autism characteristics
The study also examined the link between MAR ASD and autism severity. It showed that children of mothers with +MAR antibodies had higher autism severity scores than those of -MAR mothers. It did not find significant differences in their IQ, adaptive function, or unusual behavior.
“MAR ASD positivity may be linked to more severe autism behaviors,” Angkustsiri said. “Both the SCQ reported by parents and the ADOS assessed by clinicians supported these findings.”
Further study is needed to understand why mothers develop these antibodies and how long these antibodies may persist. Testing for MAR ASD patterns can be used to assess the probability of a child having autism before characteristics are present. The researchers aim to develop an accurate clinical test to provide clinicians with more tools for an earlier diagnosis of ASD.
“We hope our work can help develop better-tailored services based on the type of autism and the child’s strengths and specific challenges,” Van de Water said.
The study was funded by the NIH/National Institute of Environmental Health Scien-ces, the Eunice Kennedy Shriver National Institute of Child Health and Human Deve-lopment, the Consejo Nacional de Ciencia y Tecnologia, and the DBPNet Young Investigator Award.
References:
“Maternal autoantibody profiles as biomarkers for ASD and ASD with co-occurring intellectual disability” by Alexandra Ramirez-Celis,Lisa A.Croen,Cathleen K. Yoshida, Stacey E. Alexeeff, Joseph Schauer, Robert H.Yolken, Paul Ashwood, and Judy Van de Water, 26 May 2022, Molecular Psychiatry. DOI: 10.1038/s41380-022-01633-4
“Pilot Study of Maternal Autoantibody–Related Autism” by Angkustsiri, Kathleen MD, MAS, Fussell, Jill J.MD, Bennett, Amanda MD, MPH, Schauer, Joseph BS, Ramirez-Celis, Alexandra Ph.D., Hansen, Robin L. MD and Van de Water, Judy Ph.D., 1 June 2022, Journal of Developmental and Behavioral Pediatrics. DOI: 10.1097/DBP.0000000000001100
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https://scitechdaily.com/what-causes-autism-new-research-uncovers-a-key-factor-in-brain-development/
" What Causes Autism? New Research Uncovers a Key Factor in Brain Development
The findings of this research reveal a significant component in the underlying causes of neural tube birth defects, intellectual disabilities, and autism risk.
Researchers from Texas A&M College of Medicine have provided answers to important questions concerning how the neocortex develops, providing new information about the root causes of intellectual disabilities.
A significant advancement in our understanding of how the brain develops has been accomplished by researchers at Texas A&M University College of Medicine. This new research advances our understanding of how the region of the brain that distinguishes humans from other animals develops and sheds light on what causes intellectual disabilities, such as autism spectrum disorders.
For many years, scientists have recognized a significant relationship between mammalian intelligence and a thin layer of cells in the neocortex, the region of the brain that governs higher-order processes like cognition, perception, and language. The neocortex’s surface area reflects how highly developed an organism’s mental ability is. For instance, the human neocortex is only around three times thicker than the mouse equivalent. However, the human neocortex has a 1,000-fold larger surface area than that of mice. Autism spectrum disorders and intellectual impairments are among the developmental deficiencies caused by malformations in this region of the brain.
What is unknown is how evolutionary expansion of this section of the brain happens selectively in favor of growing the neocortex’s surface area at the cost of increasing its thickness. An important aspect of this process is how the initial populations of neural stem cells, which serve as the brain’s building blocks, distribute themselves.
“There are many, what we’ll call, individual processing units that are horizontally arranged in the neocortex. The more surface area you have, the more of these processing units you can accommodate,” said Vytas A. Bankaitis, Distinguished Professor at the College of Medicine, E.L. Wehner-Welch Foundation Chair in Chemistry, and co-author of this study, which was published in Cell Reports. “The question is, why is the neocortical surface area so much greater relative to its thickness as one climbs up the mammalian evolutionary tree? Why do neural stem cells spread themselves in a lateral direction as they proliferate and not pile on top of each other?”
This question is key because when the cells do not spread out, but instead pile up, it creates a thicker neocortex with a smaller surface area - a characteristic that has been observed in cases of intellectual disability and even autism.
“One of the most studied genetic causes of intellectual disability is a mutation in a gene that was originally called LIS1,” said Zhigang Xie, assistant professor at the College of Medicine and co-author of the study. “This genetic mutation will cause a smooth brain, which is associated with intellectual disability. And one typical observation is that the neocortex of the patient is thicker than normal. There are also very recent studies that identify common differences in the brain of autism that include abnormally thickened regions of the neocortex in those individuals.”
Scientists have known for some time that as neural stem cells divide, their nuclei move up and down within their anatomical space as a function of the cell cycle, a process called interkinetic nuclear migration. They do so by employing a cytoskeletal network that acts like train tracks with engines that move the nuclei up or down in a closely regulated manner. Although several ideas have been proposed, it remains an enigma why the nuclei move in this way, how this network of train tracks is controlled, and what role interkinetic nuclear migration plays in development of the neocortex.
In their study, Xie and Bankaitis provide answers to these questions.
As for why, Bankaitis explains that when there are so many cells so close together in the embryonic stage of neocortical development, the movement of their nuclei up and down causes opposing upward and downward forces that spreads the dividing neural stem cells out.
“Think about a tube of toothpaste,” Bankaitis said. “If you were to take that toothpaste tube, put it between your hands, push up from the bottom and push down from the top, what would happen? It would flatten and spread out. That’s essentially how this works. You have an upward force and a downward force caused by the movement of the nuclei that spreads these cells out.”
Xie and Bankaitis also demonstrate how the cells do this by linking together several distinct pathways that cooperate to “tell” the newborn neural stem cells where to go.
“I think for the first time, this really puts together molecules and signaling pathways that indicate how this process is controlled and why it would be linked or associated with neurodevelopmental deficiencies,” Bankaitis said. “We have taken a biochemical pathway, linked it to a cell biological pathway, and linked it to a signaling pathway that talks to the nucleus to promote the nuclear behavior that generates a force that develops a complicated brain. It’s now a complete circuit.”
The results of this study uncover an important factor in the underlying causes of autism risk, intellectual disabilities and neural tube birth defects. The new knowledge on the basic principles regulating the shape of the neocortex will also help the design of in vitro brain culture systems that more accurately reflect the developmental processes of interest and improve the prospects for neurological drug development.
“While there might prove to be many reasons why a neocortex thickens instead of spreads, our work provides a new perspective on why patients with autism and intellectual disabilities often display a thicker cortex,” Xie said. “The fact that the LIS1 gene product is a core regulator of nuclear migration, including the interkinetic nuclear migration that we study in this work, supports the conclusions we reach in this paper.”
Reference: “Phosphatidylinositol transfer protein/planar cell polarity axis regulates neocortical morphogenesis by supporting interkinetic nuclear migration” by Zhigang Xie and Vytas A. Bankaitis, 31 May 2022, Cell Reports.
DOI: 10.1016/j.celrep.2022.110869
The study was funded by the NIH/National Institutes of Health and the Robert A Welch Foundation. "
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https://scitechdaily.com/new-research-could-change-our-understanding-of-autism/
" New Research Could Change Our Understanding of Autism
It is commonly believed that autistic individuals are worse at recognizing other people’s emotions. Could this belief be false?
Research on identifying facial emotional expressions may alter how we see autism.
There is a widespread belief that autistic people are poor at recognizing the emotions of others and have little insight into how effectively they do so.
However, a recent Australian study has demonstrated that individuals with autism are just slightly less accurate than their non-autistic peers at recognizing facial expressions of emotion.
Recent research shows we may need to reevaluate widely held beliefs that adults with autism experience difficulties with social emotion recognition and have little insight into their processing of other people’s facial expressions. The findings were recently published in the journal Autism Research.
In a Flinders University study, 63 individuals with autism and 67 non-autistic adults (with IQs ranging from 85 to 143) took part in three 5-hour sessions comparing their identification of 12 human facial emotion expressions such as anger and sadness.
During her Ph.D., Dr. Marie Georgopoulos gathered a broad range of data, with later reanalyses by the research team serving as the foundation for a series of research papers.
The results could mean social difficulties linked with autism may actually reflect differences that only become apparent in certain social interactions or high-pressure scenarios, challenging the perspective that autistic adults can’t adequately read facial emotion expressions.
Study co-author and Matthew Flinders Distinguished Emeritus Professor of Psychology, Neil Brewer, says by deploying a wide array of emotions, presented in a variety of different ways, this study suggests that autistic individuals are, on average, only slightly less accurate but at the same time somewhat slower when classifying others’ emotions.
“These findings challenge the notion that adults with autism are more likely to be overwhelmed by increasingly dynamic or complex emotional stimuli and to experience difficulties recognizing specific emotions.”
The differences between groups were consistent regardless of how emotions were presented, the nature of the response required, or the particular emotion being looked at.
The research also showed that while there was considerable variability in terms of individuals’ insight into their interpretation of others’ emotions, there was no evidence of any differences between the autistic and non-autistic samples.
“The sophisticated methodologies used in these studies not only help refine our understanding of emotion processing in autism but also provide further demonstrations of hitherto unacknowledged capabilities of autistic individuals.”
Reference: “Facing up to others’ emotions: No evidence of autism-related deficits in metacognitive awareness of emotion recognition” by Neil Brewer, Carmen A. Lucas, Marie Antonia Georgopoulos and Robyn L. Young, 7 July 2022, Autism Research.
DOI: 10.1002/aur.2781
The study was funded by Flinders University.
“Further advances will likely require us to tap behaviors associated with emotion recognition and reactions to others’ emotions in real-life interactions or perhaps in virtual reality settings.”
There was considerable overlap in performance between the two groups, with only a very small subgroup of autistic individuals performing at levels below that of their non-autistic peers.
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