Friday, 26 January 2018

Ambitious about Autism? All roads lead to Las Vegas

There are many odd things in the world of autism. One is ABA (Applied Behavioral Analysis), the gold standard therapy in North America, where it is seen as evidence-based.  In the rest of the world there is very little ABA and that same “evidence” is not seen as conclusive.
Raymond in Las Vegas with his “assistant” Charlie

In the US, Federal Government funded very early intensive intervention is available to anyone under three years old with an autism diagnosis. The “evidence” shows that such very early intervention can change the outcome.  But why stop at three years old? What is magical about 36 months of age? After this age some people continue to get intensive intervention and some do not; it all depends where you live and who wants to pay.
If the evidence is so strong that very early intervention is so effective, why do rich European countries leave it to far older than 36 months to even diagnose autism?
Much does not add up in the world of autism.
Personally, I am a fan of ABA as a teaching method, but only when done in a fun way, which is how our US-trained Behavioral Consultants practised it. Lots of high fives, “good jobs”, smiling faces, tickling, dancing and generally a good time; no tears and no stress.
I cannot see why you would stop your intensive intervention so soon after starting it and I really doubt you make a life-changing difference very often, by 36 months of age.
One of our Behavioral Consultants came from the New England Center for Children and I recall asking her, “so when do you stop with your therapy?” She told me that they have people in their 60s still in therapy and they might go on a trip with their assistant to Las Vegas (yes, just like in Rain Man).   
There are many special schools in the US using techniques like ABA. Because of the high ratio of staff to pupils, these schools are very expensive and somebody has to pick up the bill.
In Europe there are very few ABA schools, one of the first is called Tree House and was established in London.  It was set up by a charity called Ambitious about Autism.  This school is very expensive and the idea is that the municipal authority where you live is supposed to pay the fee for you. This would come out of their budget for special needs kids, so the more money they spend on such private schools the less money there is left over for the kids with less demanding parents, who do not advocate for their kids.
Anyway, I recently came across the fact that Ambitious about Autism has gone a step further and now runs Ambitious College for people up to the age of 25.
This made me wonder if you go to the ABA school from 4 to 18 years old and then go to the ABA college until you are 25, when does it end? Perhaps with a trip to Las Vegas? 

ABA as a treatment or a teaching method
While I see ABA as a (highly effective, in the right hands) teaching method, the ABA specialists put if forward as a proven treatment, meaning you should get better. 

Ambitious or Realistic?
When treating a three year old with autism I think you have to be ambitious, optimistic and hopeful.
At some point I think you need to be realistic.
Day care and activities for young adults with severe autism is a great idea. Including them in activities with non-autistic people would be even better.
With people living longer there are many activities for retired older people, which are entirely suitable for adults with (non-violent) severe autism, or indeed with Down Syndrome.  Why can’t the 25 year old with severe autism play table tennis with the 70 year old retired teacher and go to the same keep fit class?  Last year Monty, aged 14 with ASD, was in Shanghai and when he saw a large group of older Chinese people doing their group exercises in a public park; he joined in. Everybody enjoyed it. 
I am not sure creating a “College” for people with severe autism is helpful. Helping people with autism go to a regular college, by giving them an assistant, is a good idea.
If it really is day care, why not call it day care?
If it is about preparing for life in the real world, what was happening at the ABA school from 4 to 18 years old?


  1. Hi all, I've found some really interesting info

    The following new paper shows the lack of microbial diversity in oral microbiota in ASD kids vs NT:

    Key section: "At the genus level, increased abundance of Streptococcus and Haemophilus, as well as markedly reduced abundance of Prevotella, Alloprevotella, Selenomonas, Actinomyces, Porphyromonas and Fusobacterium in ASD samples were observed, suggesting a characteristic dysbiotic signature. The family Prevotellaceae, including the genera Prevotella and Alloprevotella, also showed a relatively low abundance in children with ASD. This was evident in dental samples as demonstrated in the co-occurrence network (Fig. 4). In agreement with these findings, Finegold et al. recorded a depletion of Prevotella in the gut of autistic patients compared to sibling controls. Meanwhile, Kang et al. reported that Prevotella, as the most significantly altered genus between autistic and neurotypical subjects, decreases dramatically in abundance in stool samples from autistic patients. A low abundance of Prevotella was also detected in feces from patients with Parkinson’s disease and untreated Multiple Sclerosis, supporting the relevance of this bacterium in CNS disorders. Prevotella is a commensal microorganism in multiple human habitats, including the intestine and oral cavity; it does not only interact with the immune system but also plays a key role in degrading a broad spectrum of saccharides. Interestingly, it was reported that autistic children may have deficiencies in saccharide metabolism and impaired carbohydrate digestion. Prevotella species also have essential genes for the biosynthesis of vitamins, which were reported to mitigate ASD symptoms. Future studies are warranted to further interrogate the role of Prevotellaceae, also evaluating its therapeutic potential for ASD."

    I then went back and looked at gut microbiome info on ASD versus NT, especially those dealing with Prevotella:

    In this paper, look at the following two images:

    Then this paper:

    Prevotella is significantly low in the gut microbiome of ASD kids, which makes the following paper very releant:

    In this study, Prevotella H. suppresses CNS inflammatory disease. Specifically "P. histicola challenge led to a decrease in pro-inflammatory Th1 and Th17 cells and an increase in the frequencies of CD4+FoxP3+ regulatory T cells, tolerogenic dendritic cells, and suppressive macrophages"

    So if ASD kids are very low on a gut microbe that helps suppress CNS inflammation, could increasing Prevotella H help?

    In fact, the university that conducted the relevant FMT protocol has applied for a few patents including:

    I have searched everywhere but can't find Prevotella Histicola for sale as a probiotic. Based on the significant improvement in my daughter after antibiotics / Nystatin with concurrent and continued probiotics, I believe the gut microbiome does play a role. I wish Prevotella Histicola was available for us to use.

    It has however made me very curious about Ubiome


  2. Hi Peter and community,

    I think this qualifies as big news:

    Roche wins FDA's breakthrough therapy label for autism drug

    ZURICH (Reuters) - Swiss drugmaker Roche said on Monday the U.S. Food and Drug Administration granted its breakthrough therapy designation for Balovaptan to treat autism spectrum disorder (ASD), potentially accelerating its development and approval.

    FILE PHOTO: Logo of Swiss drugmaker Roche is seen beside the entrance of its research unit Roche Glycart AG in Schlieren, Switzerland December 18, 2017. REUTERS/Arnd Wiegmann/File Photo
    Balovaptan, which may improve social interaction and communication in people with ASD, is being developed by Roche’s Swiss-based pRED research unit and has an expected filing date of after 2020, according to the company’s website.

    Autism spectrum disorder has no standard FDA-approved drugs for its core symptoms such as social interaction difficulties, communication challenges and a tendency to engage in repetitive behaviors. Roche said Balovaptan has shown the potential to improve social interaction and communication in people with ASD.
    “We look forward to working closely with the FDA in the hope that we can bring this medicine to these individuals as quickly as possible,” said Roche Chief Medical Officer Sandra Horning.
    Roche’s pRED research and development unit has historically lagged the output of its California-based Genentech unit, the source of nearly all its biggest sellers.
    Still, the Basel-based company has begun highlighting several pRED medicines, including Balovaptan, as among its top drug prospects.

    Just saw this, will dig a bit further, but very interesting on the surface.


    1. AJ, this drug targets Vasopressin receptor 1A, encoded by a gene nicknamed the 'Ruthlessness gene'.

      The idea is that a little extra vasopressin makes people behave nicer. It is very similar to Oxytocin.

      Outside the brain there will be many other effects that may not be so helpful; you would want a brain specific drug.

      You probably can achieve a similar effect to the new drug Balovaptan with a vasopressin nasal spray.

    2. Interesting, but keep in mind that blocking vasopressin on a receptor like 1A could give cognitive problems as vasopressin itself is a cognition enhancer.

      Not to mention vasopressin is needed for males, blocking it out commpletely will almost certainly annihilates any guy his drive to go after a girl.

      Im sure there are some that benefit from antagonism, where others who have lack of social desire would benefit more from agonism.

  3. This article may give you a rough idea about V1AR, Vasopressin, Balovaptan and Oxytocin:

    I am a bit confused how blocking the V1AR would achieve the similar effect as increase the level of vasopressin...

    "Roche’s approach is rather different, speculating that blocking the activity of the hormone at one receptor will help improve social functioning and avoid potential side effects of increasing vasopressin across the board, which some scientists believe could lead to increased aggression.

    In a study in adult males with autism, balovaptan showed a trend towards activity on social functioning scores but failed to reach statistical significance but was able to achieve a significant improvement on an adaptive behavior rating scale at higher doses."

    Anyway I doubt is it useful for ASD...

  4. New articles on sirtuins (=Class 3 HDACs):

    "Honokiol significantly enhanced SIRT3 expression, reduced reactive oxygen species generation and lipid peroxidation, enhanced antioxidant activities, and mitochondrial function thereby reducing amyloid βeta (..) Honokiol increased the expression of AMPK, CREB and PGC-1α, thereby inhibiting β-secretase activity leading to reduced Aβ levels."

    "Previous study has shown that adjudin, a potential Sirt3 activator, could attenuate lipopolysaccharide (LPS)- and stroke-induced neuroinflammation () Both our in vivo and in vitro results showed that adjudin reduced astrocyte activation by upregulating Sirt3 expression. In addition, adjudin treatment after stroke promoted functional and neurovascular recovery accompanied with the decreased area of glial scar in WT mice () previous studies have shown that both Sirt1 activator and Sirt2-selective inhibitor were able to attenuate the activation of astrocyte as well as the production of proinflammatory cytokines () We found Notch1 signaling pathway could be inhibited by adjudin accompanied with increased Sirt3 both in vivo and in vitro."


    "Bergenin, isolated from the herb of Saxifraga stolonifera, has anti-inflammatory, antitussive and wound healing activities. () Bergenin obviously inhibited the mRNA and protein expressions of IL-6 and TNF-α in colon tissues, but not that of mucosal barrier-associated proteins occludin, E-cadherin and MUC-2 () bergenin was identified as a PPARγ agonist () In addition, bergenin significantly up-regulated expression of SIRT1, inhibited acetylation of NF-κB-p65 () bergenin could ameliorate colitis in mice through inhibiting the activation of macrophages via regulating PPARγ/SIRT1/NF-κB-p65 pathway."



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