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Science Autism

mr peabody

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Kiwi retailer launches 'quiet hour' for autistic shoppers

Medical Xpress | Oct 31 2019

Kiwi retailer launches 'quiet hour' for autistic shoppers

New Zealand's largest supermarket chain has introduced a "quiet hour" to help make shopping less overwhelming for people with autism and other sensory processing disorders.

Every Wednesday afternoon, Countdown supermarkets dim the lights, silence background music, restrict PA announcements to emergencies only and temporarily halt shelf stocking.

"Even the ding of checkout tills is dialled down to a minimum, and strip lighting in freezer aisles is switched off to stop the low-level neon hum," Countdown manager Kirsten Dinnan said.

"It creates an environment a bit like a library," she told AFP. "We find that people tend to self-regulate and shush themselves."

The idea for quiet hour emerged last year when Dinnan was looking for ways to help the community in the rural North Island town of Marton, where she was managing the local supermarket at the time.

A member of her staff, Theo Hogg, suggested the change after experiencing difficulty shopping with his severely autistic son Hunter.

"A lot of us take ducking in and out of the supermarket for granted, but for those with sensory processing disorders it can be overwhelming because there are so many triggers," she said.

"It can cause a meltdown of epic proportions. Ten or 15 years ago, we'd have said that's a naughty child, but there's more understanding now and we want to create a judgement-free zone."

Dinnan said the response to a trial in several stores had been "overwhelmingly positive", resulting in the initiative being introduced nationwide this month in Countdown's 180 supermarkets.

"It highlights how some small changes can create a more inclusive environment that will impact people significantly," Autism New Zealand chief executive Dane Dougan said.

Supermarkets in Australia and Britain have introduced similar measures, although it is unclear where the concept originated.

Dinnan said the trial had not only benefitted the autistic community but other shoppers such as families with young children, the elderly and people who were recovering from strokes or head injuries.

"It's great if we can reduce the stress in people's lives and make an everyday experience a bit easier for them," she said.

 

mr peabody

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Behavioral disorders in kids with autism linked to reduced brain connectivity

Neuroscience News | April 19, 2019

Reduced connectivity between the amygdala and ventrolateral prefrontal cortex has been identified in children on the autism spectrum who exhibit disruptive behaviors, compared to those on the spectrum who do not. Findings suggest this distinct brain network could be independent of core autism symptoms.

More than a quarter of children with autism spectrum disorder are also diagnosed with disruptive behavior disorders. For the first time, Yale researchers have identified a possible biological cause: a key mechanism that regulates emotion functions differently in the brains of the children who exhibit disruptive behavior.

“Disruptive behaviors such as aggression, irritability, and noncompliance are common in children with autism, and are among the main reasons for psychiatric treatment and even hospitalization,” said Denis Sukhodolsky, senior author and associate professor in the Yale Child Study Center. “Yet, little is known about the biological underpinnings of behavioral problems in children with autism.”

The first of its kind, the Yale study used fMRI scans conducted during an emotion perception task to compare the brain activity of autistic children who do and do not exhibit disruptive behavior. While in the scanner, the children were asked to view pictures of human faces that displayed calm or fearful expressions.

During the task, the researchers found reduced connectivity between the amygdala and ventrolateral prefrontal cortex — a pathway critical to the regulation of emotion — in the brains of children who exhibit disruptive behavior as compared to the brains of children who do not. “Reduced amygdala-ventrolateral prefrontal cortex functional connectivity was uniquely associated with disruptive behavior but not with severity of social deficits or anxiety, suggesting a distinct brain network that could be separate from core autism symptoms,” explained Karim Ibrahim, first author and postdoctoral fellow in the Sukhodolsky lab.

“This finding points to a brain mechanism of emotion dysregulation in children with autism and offers a potential biomarker for developing targeted treatments for irritability and aggression in autism,” said Sukhodolsky.

 

mr peabody

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How is Asperger’s different from Autism?

by Julie Marks

When you think of autism, you might picture a child who is nonverbal and has a lower IQ. But this isn’t necessarily the case for kids with Asperger’s syndrome.

There’s no specific Asperger’s test to tell the difference between Asperger’s and autism, but many experts agree that the two disorders each prompt distinct behaviors.

From the way they communicate to the way they learn, people with Asperger’s and autism face unique challenges but also have exceptional gifts.

Asperger’s: Does it even exist anymore?

You should know that Asperger’s isn’t officially recognized as its “own” syndrome anymore.

The American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5) no longer considers Asperger’s syndrome a separate disorder. Since 2013, doctors have been instructed to diagnose Asperger’s and autism both as “autism spectrum disorders.”

Despite this newer classification, many experts believe that children and adults with Asperger’s have clear-cut symptoms that set them apart from those with autism. Indeed, the “lumping” of autism spectrum disorders has caused quite a bit of debate in the medical community.

Difference No. 1: There’s rarely a language delay

One big difference between autism and Asperger’s is that kids with autism tend to start talking later. Those with Asperger’s usually don’t experience a language delay.

While children with autism often seem aloof, those with Asperger’s usually want to interact with others.

Though they welcome conversation, kids with Asperger’s do find it difficult to communicate and may come off as socially awkward.

Difficulty maintaining eye contact and reading facial expressions, and speaking without emotion are signature traits of Asperger’s. Children and adults with Asperger’s find it difficult to recognize and express their own feelings.

Difference No. 2: IQ may be higher than normal

While kids with autism typically have a below average IQ, those with Asperger’s may have higher-than-normal intelligence.

Some children with Asperger’s have a very advanced vocabulary and may become experts in memorizing facts about a specific subject. For instance, they may remember and recite specific sports statistics or facts about dinosaurs.

Some kids with Asperger’s are described as “gifted” and having intellectual talents. They may perform exceptionally well academically, but this isn’t always the case, as many also have behavioral problems that can hold them back.

Difference No. 3: Time of diagnosis

The average age of diagnosis for a child with autism is around age 4.

Because kids with Asperger’s typically don’t exhibit language delays or have lower IQs, they’re often misdiagnosed or not diagnosed until much later, sometimes in the teen or adult years.

Many parents may not realize that their son or daughter has Asperger’s until he or she starts interacting with peers or participating in social activities.

Asperger’s is often misdiagnosed as attention deficit and hyperactivity disorder (ADHD). Although these conditions are sometimes both present, Asperger’s is different from ADHD in that it’s a problem with socializing, rather than a problem with focusing attention.

Difference No. 4: Their brains are wired and shaped differently

Some research has suggested that children with Asperger’s syndrome have different brain patterns than those with autism.

In one study, scientists used electroencephalography (EEG) to measure the amount of signaling that occurs between brain areas of children with Asperger’s and those with autism.

Kids with Asperger’s syndrome displayed different patterns of brain activity, which suggests differences in the way their brains are connected. Specifically, children with Asperger’s may have stronger connections in the left hemisphere of the brain compared with autistic children.

Other researchers have found that a region of the brain that controls language has more folds in children with autism than in kids with Asperger’s.

While this research offers intriguing clues about how the brains of people with autism and Asperger’s may be different, more studies need to be done. Investigators continue to explore the brains of children to reveal more information.

Difference No. 5: Less severe symptoms in Asperger’s

Some experts describe children and adults with Asperger’s as having “high-functioning autism.” While this exact terminology is often debated, it’s true that those with Asperger’s generally experience less severe symptoms than those with autism.

Because of this, people with Asperger’s are often able to live independently and may be able to attend mainstream schools where they can excel academically. Conversely, many kids with autism will need specialized education and support, although this isn’t always the case.

How Asperger’s and Autism are similar

While there are some differences between Asperger’s and autism, the disorders share a lot of the same symptoms. Children with both conditions may have:

- Difficulty maintaining relationships
- Problems expressing feelings or emotions
- Trouble maintaining eye contact
- Sensitivities to certain foods or sounds
- Issues with motor skills
- A desire to follow strict schedules
- An obsession with specific subjects

Both kids with autism and those with Asperger’s may be perceived by others as “awkward” in social situations. Additionally, engaging in hand-flapping (rapidly waving hands in the air) is common in those with both disorders.

The bottom line: Both disorders require intervention

Sometimes, there’s not an obvious difference between a child with Asperger’s and one with autism. Signs and symptoms can overlap, and doctors may not make a distinction between the two disorders.

Because the newer diagnostic criteria lumps the conditions together, you may be told that your child has an “autism spectrum disorder,” instead of “autism” or “Asperger’s.”

Also, every child with an autism spectrum disorder is different. He or she may not have the same symptoms as another child.

Your doctor can help you determine specific traits that may further categorize your child. But, for the most part, kids with Asperger’s syndrome and autism face similar challenges and benefit from similar treatment approaches.

The takeaway for parents is to tell your doctor if you notice the signs of Asperger’s or autism. Both disorders benefit from early intervention. The sooner you can spot and treat an autism spectrum disorder, the better your chances for a good outcome.

https://www.everydayhealth.com/aspergers/how-aspergers-different-than-autism/
 

MountainTrails

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I have an intro post over in the New Members section, which might be useful in understanding what I’m trying to do.

But basically, I’m interested in having a conversation on the effects of various substances on autistic individuals, especially those effects you consider atypical, and what you think might be going on.

I’m also wary of dumping a massive initial post here with too many words.

My own atypical experiences leave some open questions where I can’t disambiguate/trim some of the possibilities, and I think that a wider data set might provide some interesting commonalities or divergences of experience.

Which substances, right? The obvious one, the one getting most of the attention, is MDMA. But I also don’t want to limit the conversation. Still, with MDMA, there does seem to be some anecdotally reported stuff that makes it a reasonable starting point.

I’ve had conversations with other autists in person about that, and there seems to be a surprisingly common element of little to no feeling of well-being, or euphoria, or whatever term you like to use to describe the usual main effect.

I’ll go into some detail re my own experience and open questions, and where I can’t disambiguate some possibilities away (a simple one, for example, maybe my current information is too limited, and skewed misleadingly). I’m hoping that as people kick in with their own thoughts, some interesting commonalities (or divergences) in experience will appear. We’ll see, eh?

But to avoid that “massive initial post” thing, I think I’ll stop right here for today. I hope you find the topic intriguing enough to engage. So, here we go … [hits “Post reply”]
 

Phoenix_rising

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Fucking hell Mr Peabody you could write a book with all this compiled information. I admittedly haven't read it all,but what I have has been very informative. My son is 9 and is on the spectrum,when he was a toddler they said he had autistic traits with global delay disorder,now they say its ASD.

I shall endeavour to read it all. Thanks for posting this.
 

mr peabody

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Pilot study finds MDMA-assisted psychotherapy significantly reduces social anxiety in autistic adults

Experiencing repeated social rejection and abuse from family and friends is a difficult part of childhood for many people, but it’s especially traumatic (and common) for children on the autism spectrum. Many of these children later develop into adults who suffer from diagnosed conditions like anxiety, post-traumatic stress disorder (PTSD), and depression, in addition to enduring challenges with interpersonal connection and social adaptability.

Conventional medications have been mostly ineffective at treating stress-related issues among the autistic population, and traditional psychotherapy is largely unsuccessful because it is typically difficult for people with autism to develop rapport with therapists. Due to these issues, effectively reducing stress for those with autism has remained a lofty goal that so far hasn’t borne many practical solutions—until now.

A new study published earlier this month in Psychopharmacology explored whether psychotherapy combined with MDMA (the primary ingredient in the street drug known as “ecstasy”) was safe and effective at treating social anxiety in autistic adults.

Rather than attempt to treat autism itself, the study aimed to find out whether the treatment method was able to relieve symptoms (such as social fear and avoidance) that contribute to the sociability and quality of life that this population commonly experiences.

The Phase 2 pilot study, sponsored by the Multidisciplinary Association for Psychedelic Studies (MAPS), marks the first time clinical research has ever been conducted on treating autistic adults with MDMA—or any other psychedelic substance, for that matter.

Giving ecstasy to adults with autism in an attempt to address their social anxiety may sound a bit foolish to some—perhaps even dangerously reckless. However, other studies have found MDMA to be effective in treating other anxiety disorders and the researchers took measures to ensure the safety of all participants.

Prior to designing the study, interviews were conducted and survey data was collected from autistic adults about their experiences with using MDMA in non-medical settings. This data showed that a majority of survey participants reported experiencing an ease of communication and heightened feelings of empathy and connectedness, both during their (unsupervised) MDMA sessions and after.

That’s because MDMA is capable of engendering benefits such as increased feelings of well-being and cultivating qualities like interpersonal trust and empathy, while also decreasing feelings of fear. So even if people use MDMA outside of the medical model, it’s possible to experience lasting benefits from safe experimentation. This assumes that they are employing tried-and-true harm reduction techniques like drug checking, avoiding dangerous drug combinations, and accurately weighing their doses, of course.

By taking part in this innovative scientific study, these autistic adults did imbibe MDMA within the modern psychedelic therapy framework.

Study Design

The randomized, placebo-controlled, double-blind single-site study occurred over the course of nearly three years—from February 2014 through April 2017. Twelve autistic adults with marked to very severe social anxiety were recruited through Internet advertisements, word of mouth, and clinician referrals. All participants were required to be 21 or older, MDMA-naive (by self-report), physically healthy, and psychologically stable.

After three 60- to 90-minute non-drug preparatory psychotherapy sessions, participants underwent two eight-hour experimental sessions, receiving either MDMA or the placebo (lactose). These experimental sessions were spaced roughly one month apart.

Eight participants received MDMA, and the remaining four participants received the placebo. As this was a double-blind study, neither the participants nor the researchers knew whether the dose was active or placebo until the blind was broken during a six-month follow-up session. Surprisingly (compared to other psychedelic research studies), it was not always apparent (to both the participants and the researchers) whether MDMA or the placebo was administered.

Following each experimental session, the volunteers participated in three additional 60- to 90-minute non-drug integrative psychotherapy sessions over the course of three weeks. Each session included mindfulness-based therapeutic techniques, which have been previously found to be useful for autistic adults and other populations experiencing issues with emotional regulation, relationships, and tolerance of distress.

This study design was similar to the methods used in researching MDMA-assisted psychotherapy for the treatment of PTSD in otherwise healthy adults, but it employed a few variations that were intended to meet the needs of the autistic population. The first four participants received MDMA in the initial session at a dose lower (75mg) than the typical full dose in PTSD trials (100-125mg), and after verifying that there weren’t any issues with the 75mg dose, the dose was increased to 100-125mg for the rest of the sessions and participants.

Also different from the MDMA-assisted psychotherapy PTSD studies, this study’s participants were not required to stay overnight in the clinic after the experimental MDMA sessions. Instead, they left with a trusted “Study Support Partner” who remained with them at home. This protocol change was made to best accommodate the needs of the autistic adults, who may have experienced elevated anxiety from staying in a clinical setting overnight.

Participants who received the placebo during the study were eligible to return for two optimal open-label treatment sessions with MDMA. Data for those additional experimental sessions were not included in the published study results.

The Results

Data from the study showed that not only is clinically-administered MDMA safe and well-tolerated in adults on the autism spectrum—there were also considerable improvements in social anxiety and improved sociability for the group that received MDMA.

Several participants and Study Support Partners described accounts of improved interpersonal interactions with family members, and some participants reported benefits like being able to start dating for the first time and becoming more comfortable with exploring and expressing gender identity.

The improvements were significantly greater for the MDMA group compared to the placebo group. More importantly, six months after the study’s conclusion, these therapeutic effects were still holding strong—social anxiety remained the same or continued to improve slightly for those participants who received MDMA.

Conclusion

Although the sample size was limited, this Phase 2 pilot study still provided more evidence supporting the idea that MDMA is capable of treating anxiety-related issues. As the first study to administer a psychedelic-related compound to the autistic population, this is truly groundbreaking research.

Due to the current legality surrounding substances like MDMA and other psychedelics, MDMA-assisted psychotherapy is not legally available to the vast majority of people who really need it. Until the laws shift, it can be helpful to research ways to access psychedelic therapy without using illegal substances. And experimenting with mindfulness techniques like meditation, yoga, and breathwork can be extremely beneficial at addressing anxiety symptoms.

Through psychedelic research studies like this one, we continue to learn more about how psychedelic substances can improve our mental health. This revolutionary research goes a long way toward finding treatments that can help the autistic population live easier, more enjoyable lives.

https://psychedelictimes.com/articles/study-mdma-assisted-psychotherapy-reduces-social-anxiety-autistic-adults/
 
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MountainTrails

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[Before posting, I talked with mr peabody about having conversation in this thread rather than just news postings. He's down with that.]

A typical experience for me goes like this:

The basics

I weigh about 175 pounds and am reasonably lean. I’m autistic (so I’ve been told by professionals, though it was at a time late enough in my life that pursuing a formal diagnosis seemed pointless) and am a visual thinker. I have some issues recognizing emotions. ("How are you feeling?" is a question guaranteed to stop me dead in my tracks for minutes while I iterate through possibilities in my head.) I was abused as a child, and live with anxiety as a close companion.

“Anonymously” obtained MDMA (sources have varied) has been tested with the Dance Safe reagent materials.

150mg to start, always on an empty stomach (3+ hours since a meal). I’m hydrated and rested.

I usually notice something about 15-20 minutes in. It will become a growing discomfort or uneasiness. I mentally categorize this as cortisol kicking in, and sitting quietly in a room with cool airflow on me helps. Rarely there is nausea, and only when I push the dosage.

Somewhere around 30-45 minutes the quality of vision/light changes. Pupils don’t show dilation but nystigmus (eye jitter) begins modestly, occasional at first but then more steady. This will continue through the experience; I find it entertaining, and I use it as a reliable and, curiously, soothing indicator of progress. There are also elements of vision that seem sharper; I associate that with an amphetamine hyperfocus.

In the 1-1.5 hour range, I redose, somewhere in the 75-150mg range. If I’m not comfortable and haven’t settled down, I don’t redose.

Somewhere in the process, my thoughts take on a floaty, wavy feeling, and if I settle back I will relax at this point. No well-being or euphoria will appear. The lights will continue to entertain and seem more liquid and rich, eye jitter will increase, music appreciation may occur, and bruxism will sometimes show itself at higher doses or later in the experience. At a higher dose, my vision has, rarely, gone double entirely. Once, I got some prickly feeling on my scalp, but it went away after a very brief appearance. I may perspire freely for a while as things progress. My pupils typically dilate little if at all until the redose, after which point some dilation is usually evident. “Big black moons”? No. But able to read the screen on my mobile device? lol. No.

During the comeup, I usually do some self-care things, such as resting quietly while leaning back on some pillows, or massaging lotion on my arms and legs, for which there’s nothing unusual about the feeling. I am aware of no increased empathy, no feeling of well-being or euphoria, no particular increase in skin sensation. Jittery eyes and music/color appreciation are the main effects, and will slowly subside. The overall experience lasts 6-8 hours.

[I’ve played some with higher doses, but exploring the performance envelope of my cardiovascular system isn’t something I’m keen on, and, well, that’s not a good road for me. FWIW, each new batch has included a restart at the dosage of 120mg in case the sourced material had changed in quality.]

Initial comments

I have described the experience as “putting me through the wringer,” but I have never had one where I could even characterize my mood as “happy.” I’ve noticed that I sometimes want to move around, not energetically but more slowly, with twisting/torsional components.

I have done this 15-20 times over the past 5 or 6 years, with consistent results although source, amount, form, and even ROA have varied.

What have I gotten out of it? The first time, I was sure I had been sold a load of crap. I was disappointed. But then days later, having gone about my life, something startled me — no, it shocked me: I found myself crying while listening to some favorite music. This was simply astounding; I don’t cry. I started to pay attention. And over time I came to the conclusion that my emotions seemed to be much closer to the surface for a while. Subsequent experiences showed me there was definitely something occurring as a result of taking this substance, and I could not understand it.

And I’ll stop there, as a natural break.
 
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mr peabody

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Children with autism and their parents participate in an early intervention program at GENIUS Kurnia in Malaysia.


Getting a new perspective on autism

by ResearchSEA | Medical Xpress | Jan 9 2019

Much-needed insight into raising young children with autism in Malaysia highlights the need to improve local research, awareness, acceptance and support services.

Raising a child with autism spectrum disorder (ASD) is challenging, and support systems can be difficult to access. In Malaysia, growing numbers of children are being referred to medical specialists, while enrollments in special needs programs doubled between 2006 and 2013. Yet most research on the condition has focused on the developed world and little is known about the experiences of parents in Malaysia.

Researchers from Universiti Teknologi MARA, Monash University Malaysia, and colleagues wanted to learn more about Malaysian parents' experiences raising children who have ASD. They interviewed 22 parents of 16 primary-school-age children with ASD about their initial reaction to their child's symptoms and diagnosis, their awareness about ASD, how family life was affected, their coping strategies and becoming resilient.

Initially, more than half the parents sought help when they noticed differences in their children's behavior or delays in development. Plans and routines were adjusted, along with expectations for their children's futures.


Children with autism and their parents participate in an early intervention program at GENIUS Kurnia in Malaysia.

Inadequacies in the medical and education system contributed to a significant amount of parental stress. They found it difficult to find support, interventions, and therapies, in part due to a lack of knowledge about autism among health professionals. Poor information and resources characterized the entire journey, from diagnosis to trying to access treatment and support.

Parents felt they faced social stigma and often felt judged or that they were labeled as a bad parent by their community due to the public's lack of awareness about the condition. One father shared his experience of his son throwing tantrums at the shopping complex: "In Malaysia, we can see that people were not so comfortable with my son's tantrums and difficult behavior. From the way they stared at us, we know."

The majority of parents said they were ignorant about autism when they first received their child's diagnosis, but they informed themselves, and more than two-thirds felt the power of knowledge helped them cope. Their resilience grew as they experienced difficulties and positive experiences from interactions within the family and their communities, and with society and government. Nearly half of the parents felt there were direct positive impacts as a result of having a child with ASD: spouses relied on each other more and became closer, while communication and a sense of connectedness improved across the family.

The researchers held workshops to share the outcomes of their study with colleagues, parents, educators, health practitioners, university students and the public. They believe their family-centric approach is crucial to understanding families with ASD, and recommend that the Malaysian government improves autism awareness across the healthcare and education sectors.

"These findings lend support to the importance of acknowledging the culture-specific components that might influence how parents perceive, give meaning and adapt," says Kartini Ilias, a clinical psychologist at Universiti Teknologi MARA. "They might also help inform parents in other Asian countries, such as Singapore, Indonesia and Vietnam."

 
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MountainTrails

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I've been seeing a lot of CBCT (cognitive behavioral conjoint therapy) articles/attention lately.


MDMA-assisted couples therapy: How a psychedelic is enhancing intimacy and healing PTSD
-- EconoTimes

Post-traumatic stress disorder (PTSD) is a mental health condition, triggered by experiencing or witnessing a terrifying or threatening event. Symptoms can include re-experiencing the trauma, avoidance, nightmares and severe anxiety. Living with PTSD can feel devastating, permanent and life-defining.

The path to relieving suffering can also feel overwhelming — diving into past pain, memories and experience to understand and move through them can be horrifying, especially when your system is screaming for you to avoid them. People’s defence systems can be so strong, their narratives about the world so stuck, that the best treatments we have available do not work for everyone.
That’s where the synthetic psychoactive drug MDMA (3,4 methylenedioxymethamphetamine) comes in — as a supportive catalyst to a therapeutic process.

MDMA has been showing excellent effect for the treatment of PTSD from many different causes — including military combat, sexual assault and childhood abuse — over the past decade, coupled with an inner-directed, supportive model of psychotherapy.

This therapy combination has received “breakthrough therapy designation” from the Food and Drug Administration (FDA) in the United States. It is currently being tested in a large, multi-site randomized controlled trial, sponsored by the Multidisciplinary Association for Psychedelic Studies (MAPS).

How MDMA works in the brain

MDMA is a drug that alters mood and perception. In non-clinical settings, it is a common recreational drug — known as Ecstasy (E) or Molly.

MDMA works on numerous neural structures (especially the amygdala and pre-frontal cortex) and enhances the secretion of hormones and neurotransmitters — namely serotonin, dopamine, norepinephrine and oxytocin, among others.

The drug can produce joyful, blissful experiences and, in the context of PTSD treatment, can allow for a revisiting of traumatic memories, emotions and context with greater ease and less avoidance than would be possible without the drug.

MDMA-facilitated psychotherapy embeds the use of MDMA within a psychotherapy treatment for PTSD, therefore providing a deeply evocative template to be able to work from — to move the seemingly immovable presence of the trauma.

Revisiting traumatic memories

As a clinical psychologist and researcher, I’ve focused my work on trauma and relationships for the past decade. As the founder of Remedy, a mental health innovation community, and an adjunct professor in psychology at Ryerson University, my goal has been to illuminate treatments for trauma that can have deep, profound and lasting effects. This is what inspired me to work with MDMA.

Our team recently conducted a pilot trial of cognitive behavioural conjoint therapy (CBCT) for PTSD in combination with MDMA, with six couples in Charleston, S.C. The therapy was successful in reducing PTSD symptoms in the majority of couples and improved their relationship satisfaction.

We are now preparing to run a pilot trial of cognitive processing therapy (CPT) with MDMA and a larger randomized controlled trial of CBCT with MDMA that will take place in Toronto, pending government and regulatory approvals.

Preparation and integration

Cognitive behavioural conjoint therapy, a treatment for couples, has demonstrated excellent effect in reducing symptoms for people with PTSD, and also for their intimate relationships and their loved ones.

Cognitive processing therapy, a treatment that focuses on meaning-making about a trauma in order to unravel thoughts and feelings that are stuck, is one of the approaches that has received the strongest recommendation in international treatment guidelines. It was also recently featured on NPR’s This American Life.

We test these highly effective trauma-focused treatments alongside the catalyst of MDMA, to see if it offers an additive or potentiating effect.
Sessions with MDMA are daylong, occurring two or three times over the course of several weeks or months, depending on the study. Research participants are accompanied by two therapists.

The therapeutic work done before the MDMA sessions prepares clients for the experience. The work afterwards integrates the experience, using the template of the MDMA session to scaffold new learnings and new ways of potentially understanding their traumatic experiences.

A life-saving legal medicine?

The large randomized controlled trial sponsored by MAPS is designed to collect enough evidence on the safety and efficacy of MDMA in treatment to make it a legal medicine.

As evidence accumulates for MDMA’s effectiveness, there is the possibility that MDMA will become legal — a medicine to be used in psychotherapy and prescribed for PTSD.

The ability to use it in practice will be potentially life-altering and life-saving for people living with PTSD.
 

mr peabody

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Standardized screening for ASD recommended at 18, 24 months

American Academy of Pediatrics | Medical Xpress | Dec 23 2019

Standardized screening for autism spectrum disorder (ASD) is recommended at ages 18 and 24 months in primary care, according to a clinical report published online Dec. 16 in Pediatrics.

Susan L. Hyman, M.D., from the Golisano Children's Hospital at the University of Rochester in New York, and colleagues updated the 2007 American Academy of Pediatrics clinical reports on the evaluation and treatment of ASD in children.

The authors note that because ASD is common, can be diagnosed from age 18 months, and has evidence-based interventions that may improve function, standardized screening for ASD at 18 and 24 months of age is recommended in primary care. Developmental screening at 9, 18, and 30 months with a validated tool is also recommended. Children should be referred for intervention at the time of identification and not wait for a diagnostic evaluation. Primary care providers should be aware of the diagnostic criteria for ASD, appropriate etiologic evaluation, and co-occurring medical and behavioral conditions that affect function and quality of life. Behavioral and other interventions to address specific skills and symptoms are supported by an increasing evidence base. Collaboration with families in evaluation and choice of intervention is recommended to promote shared decision making.

"There is no reason to wait for a diagnosis of autism before starting some services, such as speech or behavioral therapies," Hyman said in a statement. "Interventions work best when they are early, when they are intense, and when they involve the family."

 
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MountainTrails

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I like the title, which adds some clarity. For me, being able to mentally separate the feeling of well-being (not there for me) from anything else going on is an important part of understanding the value in this substance, especially for autists.


MDMA’s social and addictive effects aren’t the same
https://www.futurity.org/mdma-social-effects-addiction-2234472/

New research in mice distinguishes the molecular pathway responsible for MDMA’s abuse potential from the one behind its propensity to make people feel sociable.

The discovery could lead to novel treatments for psychiatric disorders marked by social awkwardness and withdrawal.

Methylenedioxy-methamphetamine—better known by its acronym, MDMA, or its street name, ecstasy—is a mind-altering drug that 3 million Americans use annually. MDMA is especially popular as a party drug because it gives people who take it a sense of well-being and makes them extremely sociable—even instilling feelings of unguarded empathy for strangers. That makes MDMA a natural fit for raves, dance parties featuring lots of densely packed, sweaty bodies and unfamiliar faces.

It may also may make MDMA a good medicine for psychiatry. It’s now in late-stage, multicenter clinical trials as an adjunct to psychotherapy for post-traumatic stress disorder (PTSD). The goal is to harness MDMA’s prosocial effects to strengthen the bond between patient and therapist. Thus, people who have experienced trauma may be able to feel comfortable reliving it through guided therapy.

Some 25 million people in the United States who suffer from PTSD could benefit from a drug capable of establishing, with a single dose in a therapist’s office, a trust level that typically takes months or years to achieve, says lead author Boris Heifets, assistant professor of anesthesiology, perioperative, and pain medicine at the Stanford University School of Medicine.

But MDMA can be addictive. Taken in the wrong settings or in repeated or oversized doses, it can have life-threatening consequences.
“We’ve figured out how MDMA promotes social interaction and showed that’s distinct from how it generates abuse potential among its users,” says senior author Robert Malenka, a professor in psychiatry and behavioral sciences.

MDMA and the brain’s reward circuitry

MDMA’s abuse potential stems from its capacity to stimulate the brain’s reward circuitry, Malenka says. “The brain’s reward circuitry tells us something is good for our survival and propagation. It evolved to tell us food is good when we’re hungry, water is good when we’re thirsty, and warmth is good when we’re cold. For most of us, hanging out with friends is fun, because over the course of our evolution it’s promoted our survival.”

A crucial connection in the reward circuitry is between nerve cells, or neurons, projecting from one midbrain structure, the ventral tegmental area, to another, the nucleus accumbens. When those neurons release a chemical called dopamine, the nucleus accumbens forwards signals throughout the brain that induce a sense of reward.

“Drugs of abuse trick our brains by causing an unnatural dopamine surge in the nucleus accumbens,” Malenka says. “This massive increase is much higher and more rapid than the one you get from eating ice cream or having sex.”

Like all addictive drugs, MDMA triggers dopamine release in the nucleus accumbens. That explains its abuse potential but leaves open the question of why the prosocial effect dwarfs that of most other abused drugs.

In the study, the researchers showed that a different brain chemical, serotonin, is responsible for this. Serotonin-releasing neurons in a brain structure called the dorsal raphe nucleus send projections to the same part of the nucleus accumbens that the dopamine-releasing neurons do. Neuroscientists have previously shown that in fact MDMA triggers the release of far more serotonin than dopamine.

Focus on social behavior

The researchers performed a number of experimental manipulations to implicate serotonin as the signaling substance responsible for promoting social behavior in mice. The scientists got the same results using male or female mice. The same effects would probably be seen in humans because the midbrain areas in question have been remarkably conserved among mammalian species over evolutionary time, Malenka says.

“You can’t ask mice how they’re feeling about other mice,” he says. “But you can infer it from their behavior.”

The researchers tested whether an “explorer” mouse given a relatively low dose of MDMA or, alternatively, a saline solution prefers to spend time in a chamber holding another mouse under an upside-down mesh cup (to keep that mouse from moving about) or in an otherwise identical chamber with a cup but no mouse. They found, consistently, that saline-treated explorer mice get bored after 10 minutes with another mouse. But an explorer mouse given MDMA sustains its social curiosity for at least 30 minutes.

“Giving MDMA to both mice enhanced the effect even further,” Heifets says. “It makes you wonder if maybe the therapist should also be taking MDMA.”

Like humans, mice like to return to places where they’ve had a good time. Chalk it up to the brain’s reward circuitry. To determine MDMA’s addictive potential, the researchers gave mice an MDMA dose equal to the one in the first experiment, but only when the mice were in a particular room of a two-room structure. The next day, the mice showed no preference for either room—evidence that at this dose, the drug hadn’t noticeably triggered the reward circuitry.

But mice given a higher MDMA dose exhibited both its social and abuse-potential effects. Further tests determined that the secretion of dopamine triggered by MDMA is not necessary for promoting sociability. Serotonin release, which the low MDMA dose triggered, was all it took.
The scientists were able to induce MDMA’s trademark sociability by infusing the drug only into the mice’s nucleus accumbens, proving this is where serotonin, whose release MDMA triggers, exerts its sociability-inducing effect.

“Where, exactly, in the brain that’s happening hadn’t been proven,” Heifets says. “If you don’t know where something’s happening, you’re going to have a hell of a time figuring out how it’s happening.”

Serotonin and dopamine

That’s what the scientists discovered next. Blocking a specific subtype of serotonin receptor that abounds in the nucleus accumbens fully inhibited MDMA’s prosocial effect. Furthermore, giving the mice a different serotonin-releasing drug that does not cause dopamine release mimicked the prosocial effects of MDMA but didn’t cause any addictive, or rewarding, effects.

The drug, fenfluramine, is the “fen” in a once-popular diet pill called fen/phen, a two-drug combination developed in the 1960s. Fen/phen was pulled off the market in the 1990s after 30% of patients taking it showed signs of heart disease, including pulmonary hypertension, a life-threatening condition.

Owing to their long-term cardiovascular and neurotoxic effects, neither MDMA nor fenfluramine would be suitable for any indications requiring daily use, the researchers caution.

But those nasty effects of chronic use would be highly unlikely to occur in the one or two sessions that would be required for patient-therapist bonding in a psychiatric setting, Heifets says.

The research appears in Science Translational Medicine.

Malenka is a co-founder of MapLight Therapeutics, a biotechnology company that is laying the groundwork for clinical trials of drug candidates that enhance sociability. Researchers from the Albert Einstein College of Medicine in New York also contributed to the study. Funding for the work came from the National Institutes of Health and the Wu Tsai Neurosciences Institute.

Source: Stanford University

Original Study DOI: 10.1126/scitranslmed.aaw6435
 

MountainTrails

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Messages
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(pick one or all):
1. Merry Christmas!
2. Seasonally and Culturally Appropriate Salutations!
3. meh

This one's super wordy, but here's my favorite part and something I think is ridiculously underrepresented in general understanding of autism:

ASD research continues to be challenged by clinical heterogeneity, a scientific term applied to the variability of symptoms found in subjects across the spectrum. Current research has identified increased diversity amongst people with autism participating in research...

"clinical heterogeneity"! What a great term. It's better than "ASD is a garbage-can diagnosis," which I've also heard and which makes the same point in an oh-so-much-less-elegant way. But as people look beyond the bewildering thicket of overlapping symptomatic behaviors to neurology, which informs and drives those behaviors, yeah: there seem to be some completely distinct neurological subtypes flopping in the same net inside the DSM-5.



Autism Science Foundation
Research Recap 2019: The Year of Preparing for the Future

https://autismsciencefoundation.org/key-autism-research/https-autismsciencefoundation-org-key-autism-research-2019-the-year-of-preparing-for-the-future/ (reference list for the article included at the link)

By Alycia Halladay, PhD, Chief Science Officer and The Scientific Advisory Board of ASF

The ASF Yearly Summary of Science highlights major research accomplishments that directly affect the lives of families with autism spectrum disorder (ASD). These accomplishments impact families in a number of ways: by affording those diagnosed and their families a better understanding of a particular behavior or biological feature; identifying beneficial treatment targets, interventions, services or resources; discovering technologies that not only identify unique characteristics of people with ASD but also offer insight as to how to better serve that population and by offering future predictions.

ASD research continues to be challenged by clinical heterogeneity, a scientific term applied to the variability of symptoms found in subjects across the spectrum. Current research has identified increased diversity amongst people with autism participating in research; in turn, this has led to a reduction across time in differences between people with a diagnosis vs. those without a diagnosis. In other words, those participating in research now show less severe features of ASD compared to 20 years ago. This reflects the inclusion of a more diverse set of people with autism, however, those on the more profoundly affected end may not see the benefits of research that predominantly includes those with completely different features of ASD. One solution proffered to rectify this challenge has been to stratify individuals with ASD into different groups for the purposes of research. Although advocates report that stratification lends itself to precisely determining the needs of specific groups and individuals, other researchers continue to cluster individuals into one group. Whether to stratify or cluster is a prominent discussion amongst scientists and advocates and could become polarizing, as both approaches affect research, basic nomenclature, services such as housing and employment and support services.


  1. Features in infancy predict adult outcomes
Multiple studies this year have linked children’s symptoms and biology in infancy to later outcomes. Motor abilities, family history, brain connectivity all can independently contribute to how a child develops over time. These outcomes include an autism diagnosis, verbal ability, and cognition in adulthood. This sort of research can be used to help prepare families and customize interventions that focus on the most debilitating symptoms of ASD.


This year, to make predictions about future ASD features, more studies used a longitudinal study design. This design is critical to autism research because it follows a group comprised of individuals diagnosed with ASD and, at times, individuals without a diagnosis in order to determine how they are affected as adolescents and adults. Whereas a longitudinal study can be expensive, complex and does not produce immediate results, the nature of its design provides clinicians invaluable data, affording deeper insights that allow them to more fully educate families by managing expectations, identifying focus areas and providing coping strategies that serve to help those with ASD live their best lives.

Longitudinal studies help parents understand their child’s reality and manage future expectations, as well as help scientists refine interventions according to the variability of groups of people with ASD. Multiple research studies have used data to group children based on trajectory, i.e. the progression from commencement, through adolescent development to adult functioning. The composition of these groups consists of those who show fewer symptoms and continue to improve vs. those less functioning who continue to decline. This year, two longitudinal studies, one conducted in the United States and one in Canada, closely examined toddlers to pinpoint and study specific factors that influence outcomes, from childhood to adulthood. In these studies, two patterns emerged: those possessing lower levels of symptoms who improve vs. those with more profound symptoms who decline.

While all groups showed improvement in daily living skills, those who presented less severe symptoms in toddlerhood and showed marked progression during adolescence also had the highest adaptive abilities as adults. Although most participants showed improvement in social communication with age, improvement varied, based on individual language ability as toddlers. Social communication impairments in 19 year olds was found to correlate with differences in language ability as early as age two. As speech improved, so did this core symptom of ASD: those with early minimal language ability showed the greatest functioning impairments as adults. Likewise, fine motor skills in infancy is a predictor of language at age 19, in that better fine motor skills in early childhood is a predictor of better command of language in adulthood. Together, these findings demonstrate that poor early motor skills and decreased language function are related to later ASD symptoms. This is a crucial identification, considering that both fine motor skills and language are target areas of early intervention and that intervention may improve ASD through adulthood.

The study of early motor function is not only vital to further understanding how it affects those diagnosed, it also offers insight pre-diagnosis in terms of how early motor function may predict a later ASD diagnosis. The Baby Siblings Research Consortium (BSRC) is a group of researchers that studies initial features of ASD in siblings of children with ASD as young as 6 weeks of age. Siblings of children with ASD have a 15x greater probability of having ASD themselves than do other children. Similar to previously mentioned studies, BSRC also concludes that fine motor abilities at 6 months can predict an ASD diagnosis in siblings and expressive language ability in younger siblings at 3 years.

Another factor BSRC researchers have employed to estimate the probability of diagnosis in children is number of siblings previously diagnosed with ASD. Those with at least 2 older siblings with ASD were found to have a higher probability of a diagnosis, as well as increased severe cognitive disabilities. Based on family history, this information is vital in helping families better understand the probability of an ASD diagnosis in future children, as well as predicting strengths and limitations future children may face.

In addition to identifying behavioral markers, the past decade of research has revealed a blossoming of early biological factors that may serve as additional predictors of diagnosis, ranging from genetic tests, salivary hormone markers and other reflections of altered development. Studies of brain structure, activity and connectivity have also proven valuable; when measured non-invasively, identified changes in activity in the frontal lobe of the brain during the first year of life have served to predict an ASD diagnosis in infant siblings. Because brain wavelengths vary, identifying and monitoring changes in the size of each different type of wavelength over the course of a year serves as valuable information in terms of not just determining an ASD diagnosis but also for further understanding brain fluctuations during that time period.

Complementary to brain activity, previous studies from the Infant Brain Imaging Network (IBIS) revealed different approaches to more accurately predicting ASD diagnosis by using measurements of brain structure and connectivity, in addition to mathematical algorithms based on the shape and function of different brain regions, as potential predictors of a later diagnosis. This year, the analysis of early brain based ASD markers has afforded scientists more precision in determining an association with brain connectivity in critical ASD brain regions, as well as an insistence on sameness and stereotyped behaviors at 12 – 24 months. Not only do these biological based markers aide in predicting later diagnosis and identifying features of ASD within a diagnosis, they have the potential to serve as objective ways to help determine specific interventions, both medical and behavioral.



2. Screening is not perfect, but it is essential

New technologies contribute to greater use of standardized measures in different community settings. At the same time, clinicians and scientists have developed new ways to use common records and tools, resulting in better identification of concerns at even earlier stages. Families and care providers should confidently screen early and often.



Biological based markers hold promise for even earlier detection of features, especially in those with a family history. However, to make predictions about not just a diagnosis but future expectations of needs as well, most care providers, physicians and clinicians rely on behavioral concerns. Right now, most families lack access to EEG machines and MRIs and expensive genetic testing is most often not covered by insurance. The reality of early detection of ASD in 2019 is that it occurs mostly in primary care settings, where physicians help to interpret results for the family. In 2019, the AAP published an update to their 2007 guidelines for screening for autism and it continues to recommend autism-specific screening at 18 and 24 months. Researchers continue to explore new ways to make this tool more accessible via technology, such as electronic tablets, whereas scientists continue to refine and improve accuracy screening tools using machine learning.

One challenge of current screening practices (and in fact, in all of ASD research) is the disparity in screening and screening results amongst distinct racial and ethnic groups. In order to address these differences, scientists are analyzing a variety of approaches fashioned to deal with these disparities and to increase access to screening tools. This includes remotely employing video based tools to capture ASD features to help identify and diagnosis ASD. These video based tools help parents identify signs by providing real life examples of parent-child interactions and by examining existing reports of developmental milestones from electronic medical records, with the goal of identifying early signs of developmental concerns as soon as possible, in as many infants as possible, regardless of race or ethnicity . Doing so will increase early diagnosis, leading to earlier intervention and increased understanding of ASD, self-awareness of symptoms and long-term improvement of services.


3. The lifespan of mental health challenges sparks new intervention possibilities


The high rate of mental health disorders in both children and adults with ASD means that a large percentage of this population and their families are burdened with enormous challenges Training community providers to deliver mental health interventions shows promise for alleviating these comorbidities. Clinicians need to be on the lookout for these psychiatric issues so people with autism receive the much-needed services they deserve.


While the core symptoms of ASD often lead to challenges in daily functioning, across the lifetime and spectrum of many individuals with ASD, co-occurring mental health conditions are a huge concern. Several older but smaller international studies provide a wide range of estimates of the prevalence of co-occurring conditions. A met- analysis and systematic review of these studies conducted in 2019 has helped to decipher the findings. The findings revealed 28% comorbidity of ADHD (higher in kids than adults), 20% for anxiety disorders, 11% for depression and 9% for obsessive-compulsive disorder. There is even overlap in brain based profiles of different diagnoses, both in terms of genetic activity and structure. These mental health issues, particularly anxiety, can lead to an acute crisis requiring hospitalization. Unfortunately, clinicians have limited knowledge and understanding of the nature of these mental health conditions in ASD, making intervention difficult. However, ASD researchers have had luck training community mental health providers to deliver interventions focused on addressing these mental health challenges. Training community based providers is a move in a promising direction, allowing more people to receive services in a variety of settings, but the efficacy of these interventions still lags behind those delivered in clinics. Understanding the high co-occurrence of mental health issues helps families and individuals both plan for later health care needs and anticipate potential mental health problems before they occur.


4. Heritable factors that influence brain development result in multiple psychiatric conditions, including autism.

Researchers have determined that of the over 100 autism genes that exist, all act on early developmental functions and lead to diverse, overlapping outcomes, including psychiatric disorders, autism, and related conditions. Some genetic influences, while rare, can help define the mechanisms that lead to brain cells in autism developing over time. Although a link has been established connecting environmental influences to this same spectrum of conditions, few studies have successfully defined their interaction. These findings have implications for interventions and could lead to strategies for mitigating symptoms
.


Given the comorbidity of mental health disorders with autism spectrum disorder, it should come as no surprise that new research reveals that ASD relevant genes act in fundamental ways that may influence multiple outcomes, ranging from ASD to schizophrenia, to ADHD, neurodevelopmental disorders and intellectual disability. Genes that act on such early and fundamental brain pathways have downstream effects on a number of brain functions, ASD being one of them. This might explain why there are so many ASD genes and why they are pleiotropic, meaning they have different functions. In fact, the list of genes associated with ASD keeps growing, as larger studies and better technology have revealed over 150 ASD associated genes. Infant siblings of children with autism also show rare and common gene variants in ASD genes that can aid in a diagnosis.

In addition, the presence of certain genetic mutations in ASD relevant genes can produce profound disabilities, which alone work to explain an ASD diagnosis. These mutations, referred to as rare genetic variants, are important to the community because their discovery has led to the creation of Patient Advocacy Groups that provide support and resources for focused research, as well as offer pathways to better understanding the basic circuitry of certain ASD behaviors. Scientists are studying these rare genetic forms of ASD to understand all forms of ASD, particularly gene expression in the brain. When compared to studies of the brains of people with bipolar disorder and schizophrenia, studies of brain tissue in people with ASD reveal overlapping genetic activity in genes that control synaptic signaling, neurotransmitter release, and immune response.. The abnormal immune signaling in the brain might result in cell damage, as evidenced by accumulation of T-cells in brain tissue. Studying the brains of people with ASD is the best way to understand the basic cellular and molecular basis of ASD, and is only possible through families who decide at the most difficult time to make the decision to donate. If you would like to learn more about the Autism BrainNet, which made these studies possible, visit www.takesbrains.org/signup.

While genetic factors are incredibly important in the diagnosis and presentation of symptoms of ASD, understanding the role of environmental factors in both the diagnosis and presentation of symptoms of ASD is crucial. One of the most studied environmental factors in ASD is exposure to air pollution during pregnancy. This year, ancillary evidence taken from additional locations via different methodologies shows a particular effect for a component in air pollution called PM (particulate matter) 2.5 (2.5 microns). Air pollution exposure may interact with maternal diabetes, which also increases the probability of ASD. Air pollution also seems to influence an ASD diagnosis more strongly in boys. It is important that public health policy address established, scientifically based environmental factors to address even smaller, but preventable, environmental factors.

There have been spurious reports of other environmental factors, but rather than look at factors in isolation, it is crucial to understand how these factors collectively influence brain development and interact with genetic susceptibility, either rare genetic or polygenic influences. Another area of convergence of environmental and genetic factors is epigenetics, often called the “second genome”. The epigenome is a multitude of chemicals and tags on the DNA genome that is responsive to environmental factors that can turn on or turn off DNA expression, as early as when the embryo is formed. ASD risk genes identified in genetic studies can also work epigenetically. The next generation of research will hopefully focus on understanding the multifactorial influences of an ASD diagnosis, how these factors affect symptoms and influence long term trajectories across neuropsychiatric diagnoses, including ASD.


5. Females with autism present features differently

Females with autism show opposite neurobiological features of autism, while also possessing some of the same core features of ASD. In females, these differences may be found in the way symptoms present or in associated features of ASD. Lack of differentiation clouds important scientific discoveries, which is why treatments and services should be sex specific.



Over the past five years, ASD research has increasingly focused more attention on identifying and understanding how autism manifests in females; this includes, but is not limited, to: genetic makeup, symptom presentation, long term trajectory and mental health issues. Females are diagnosed 4x less often but also have an increased load of genetic mutations, including recessive mutations. This year, results of studies have been mixed in terms of the magnitude and nature of sex and gender related symptom presentation in males vs. females, noting a problem plaguing ASD research mentioned earlier: heterogeneity. Differences across sex and gender are not seen in terms of presence or absence of symptoms, but rather in the way they present across different ages. On the whole, differences are few in infants and toddlers but are magnified during adolescence, even in the way people perceive ASD symptoms in males and females. Some scientists suggest that associated symptoms are most likely to present differently than core symptoms of ASD, with females showing a higher prevalence of ADHD and OCD, leading to differences in the way males and females appear.

In addition to findings of increased numbers of recessive mutations in the genome of females, analysis of brain structure has revealed sex differences further suggestive of the female protective effect. Focused study of the cerebellum has revealed that female activation patterns oppose those of males with ASD and fail to evince similar patterns of connectivity across different brain regions, i.e. females with ASD show reduced connectivity compared to females without ASD, an effect not seen in males with ASD. In addition, when comparing twins, females had more profound differences in the sizes of brain regions compared to males. These findings have led researchers to refine how they examine the role gender plays in basic science research.

Animal model research suggests that environmental exposures may not produce the same impairments in male vs. female offspring. Taken together, these biological findings demonstrate that females, despite demonstrating a lower prevalence of ASD, also show complicated behavioral features and more biological markers for ASD. Future research must focus on why females are diagnosed less often than males and why, when they are diagnosed, they present more behavioral markers than their male counterparts.




6. It takes a village to make interventions work in the classroom

Teachers play a considerable role in identifying and helping kids across the spectrum, which is why teachers need focused training and support in order to best serve students with ASD.



Teachers and school administrators must perform a multitude of duties and responsibilities in an effort to meet the needs of students of varying abilities within the same classroom and provide all students – those on the spectrum and those who are not – with an equal opportunity to learn. In a perfect world, each student in our school systems would receive exactly what he or she needs, when it is needed, regardless of school systems and across different symptom presentation. Unfortunately, in 2019, researchers documented that in some states, the diagnosis of ASD does not necessarily correspond to the educational classification, an inconsistency which might create disparities in service utilization across states, particularly considering that the quality of programs in many school systems rate just above adequate60.

Adding to these challenges in schools, research shows that students with ASD who exhibit unclear symptom presentation are likely to receive different services. Teacher perception of what is effective often dictates what kind of evidence-based interventions are used in the school system. Therefore, the specific types of support services students need in order to be successful often do not match up to what they actually receive. Studying clinic-based interventions in real world settings, such as in schools, is challenging as well. The biggest problem is that these interventions don’t always translate fluidly from clinic to classroom and often require modifications just to get them into the classroom. For example, according to research, a popular curriculum called TeachTown, commonly used by classroom teachers, does not necessarily help kids with ASD. The good news is scientists are using opportunities like recess65 for social interventions in ASD.

Of real concern is that the types of educational based interventions can vary based on ethnic group, leading to inequity in services. While racial and ethnic disparities continue to exist, researchers are exploring different methods to alleviate these differences. While Medicaid waivers have been shown to be somewhat helpful, most research so far has focused more on defining the problem, so that future studies can be set up to address these challenges directly. Transition to employment in the school system can be improved by the perspectives of those that have successes and challenges with employment. This includes starting early and help build environmental supports for future success on the job. These findings will lead to more tailored and effective intervention strategies to improve services for all people across the spectrum in schools, where they are desperately needed.


7. Model systems of autism are used to understand the earliest, fundamental features of ASD.

Scientists use animals and cells to determine what happens at the onset of autism and when it happens, beginning with the moment the cells are formed, in order to better build interventions for different times in development
.


Animals do not have ASD. Cells in a dish do not have ASD. But animals and cells can still provide important insight into not just therapeutic targets but can also offer a comprehensive understanding on what is happening in the brains and bodies of people with ASD. The cells in a dish actually come from cells in a person, including those with idiopathic and rare genetic forms of ASD. By using induced pluripotent stem cell (iPSC) technologies to transform a skin cell into a brain cell and then back into a skin cell, important discoveries about individual brain development can emerge. These models have revealed that certain genes cause neurons to be overconnected69 while others can impair the strengths of those connections or reduce neuronal activity on the cellular level. These are the basic fundamental properties of cell development that seem to be common across multiple psychiatric conditions, including autism.

In turn, animal models allow for a more complex analysis of single genes in the presence of organisms with other genes. Together with findings in brain tissue, these animal models have shown that, despite the gene involved, there are converging networks that could be the target of future interventions. Animal models can also demonstrate which gene x environment interactions exacerbate symptoms or alleviate symptoms in a controlled setting. They have also been able to identify the underlying molecular mechanisms of genetic mutations associated with ASD. Beyond the brain, these new models can identify mechanisms of associated dysfunction like gastrointestinal function which plague many families with ASD. A new technology introduced last year called CRISPR allows researchers to better target genes one at a time or in combination to better understand the roles of genes as well as gene x environment interactions on basic functioning of cells across the body and what this means for humans, helping them both understand and anticipate specific symptoms across time.


8. While scientists now know more about interventions, there is much that they still need to learn.

While the efficacy of fluoxetine for repetitive behaviors has been addressed, other treatments such as fecal transplants, stem cell transplants and cannabidiol still lack an evidence base and therefore use is not recommended at this time. The autism community should be cautious of interventions that lack strong scientific research, as well as by wary of flashy headlines



This year, advances in behavioral interventions for ASD revealed a common theme: remote delivery. This includes development of telehealth methods and videoconferencing. As mentioned earlier, this methodology will expand coverage while striving to ensure quality. However, findings also demonstrated what does not work. For example, fluoxetine, or Prozac, has proved to be ineffective for repetitive behaviors in ASD however that does not mean people should go off of their medication if it is helping them in other areas, but instead they should be aware that it may not help the core symptoms of ASD. On the other hand, new research in other drug targets, including the vasopressin receptor, showed promise in males. While more work needs to be done, scientists have a better understanding of what works for particular symptoms in specific people.

Although much is known, there is a great need to acknowledge emerging fields where little is known, especially in the field of intervention. Media reports hyping the effectiveness of stem cell studies and fecal transplants pushed these alternative treatments into public view however, the designs were subject to bias or had small sample sizes, suggesting further caution when considering these alternative, non-evidence based approaches. On the other hand, the target of the fecal transplants, the microbiome, has been understudied in basic and clinical studies. Probiotics have also led to improvements in gastrointestinal function in people with ASD, providing evidence that the microbiome is important but needs further study, both in determining mechanism in model systems and more precise intervention therapies.

Another alternative therapy used by families with no substantial scientific evidence is medical marijuana, including the psychoactive component THC and a non-psychoactive chemical within the cannabis plant called CBD. Unfortunately, again, media hype and marketing strategies have provided hope where scientific evidence is lacking. Research in this area is hampered by legal and administrative policies, but newer, more definitive research studies are in progress. While there is reason to be hopeful in this area, there is also reason to be cautious. People with ASD respond differently to CBD than those without ASD, and parents should not assume what works in one child without ASD will work in their child with ASD.

The Autism Science Foundation recognizes that there is much scientific information available from multiple sources that can be accessed on multiple platforms. This summary is meant to highlight this year’s advances, including differences that have changed over time and across sex, as well as shed light on similarities with other neuropsychiatric disorders. It is hard for anyone to make sense of it all when it is announced, or even as these discoveries build on each other. However, it’s important to know that advancements in understanding the basic biology of ASD have led to more specific interventions, increased knowledge of what works and what does work, further expansion in utility across settings and lastly, clues for future studies. Although this summary does not capture every insight and advancement revealed in scientific studies of ASD this year, ASF feels that these highlights offer a comprehensive overview and it will continue to share science news throughout 2020, particularly what is most valuable in helping family members understand how to best serve loved ones with ASD and themselves.
 
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Wilson Wilson

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I have an intro post over in the New Members section, which might be useful in understanding what I’m trying to do.

But basically, I’m interested in having a conversation on the effects of various substances on autistic individuals, especially those effects you consider atypical, and what you think might be going on.

I’m also wary of dumping a massive initial post here with too many words.

My own atypical experiences leave some open questions where I can’t disambiguate/trim some of the possibilities, and I think that a wider data set might provide some interesting commonalities or divergences of experience.

Which substances, right? The obvious one, the one getting most of the attention, is MDMA. But I also don’t want to limit the conversation. Still, with MDMA, there does seem to be some anecdotally reported stuff that makes it a reasonable starting point.

I’ve had conversations with other autists in person about that, and there seems to be a surprisingly common element of little to no feeling of well-being, or euphoria, or whatever term you like to use to describe the usual main effect.

I’ll go into some detail re my own experience and open questions, and where I can’t disambiguate some possibilities away (a simple one, for example, maybe my current information is too limited, and skewed misleadingly). I’m hoping that as people kick in with their own thoughts, some interesting commonalities (or divergences) in experience will appear. We’ll see, eh?

But to avoid that “massive initial post” thing, I think I’ll stop right here for today. I hope you find the topic intriguing enough to engage. So, here we go … [hits “Post reply”]
I have high functioning autism and I absolutely get euphoria from MDMA but what it also does it makes me more social and emotional and open with those emotions. Which I guess is what it does for everyone, nothing special, except I normally feel emotionally numb and unable to connect to anyone and MDMA just brings up all these feelings in me that are usually just not there. I've been able to open up and express things I couldn't even put into words before.

Of course I've also done MDMA and just blasted music and walked through stingy nettle because at the time "it felt nice" while rubbing my face and gurning my jaw off so ya know it depends what mindset you wanna take with it haha.

Generally I think most drugs seem to affect me the same as most people. But what I get out of psychedelic experiences is a whole range of emotions and thoughts I simply cannot access otherwise. LSD is my favourite full on psychedelic and it really helps me to introspect and empathise with situations from other's point of view which I otherwise just cannot do.

Again I don't think the effect a trip has on me is different from other people, it's more like the effects of drugs like MDMA and LSD are more meaningful to me because the parts of my mind they open up are parts that are so closed off normally.

I see psychedelics as internal therapy sessions.

To end this on a positive note: I honestly believe people on the high functioning end of the spectrum have a gift that gives them the potential to do better in life than most NT's. Focus your energy on what you are good at especially if it is tech related. When I was a kid they thought I wouldn't be able to get a job at all. They were very wrong and I will make more money than the idiots who said that about me (if I'm not already). I don't think most people could have predicted how important computers were gonna be and will continue to be. And do you think Silicon Valley is full of NT's? Me neither.
 

mr peabody

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‘You understand him, help him, celebrate him’ ... Chitra with Emma


Thank you to … my autistic son's teacher, to whom I'm grateful every day

by Chitra Ramaswamy | The Guardian | 29 Dec 2019

In this series we celebrate people who have had an impact on their lives. Chitra Ramaswamy thanks her autistic son's special ed teacher, Emma, for her unwavering commitment to meeting the needs of her child.

Dear Emma,

How funny that it feels entirely normal writing to you. We already write to each other, I realise with a jolt of familiarity, every single day of term. In the age of email, I know your handwriting as intimately as my own. When my son arrives home I fall on his bag with a hunger – OK, nosiness – reserved for parents seeking news of their child’s average, hopefully unremarkable school day. I rummage through the detritus of a half-eaten lunch (still not going for the sandwich, apples obviously gone) and find the diary in which our entries appear.

How I anticipate this small, thrilling exercise book, which has become a mainstay of family life, filled with the ongoing conversation between you – our son’s teacher – and us, his parents. How grateful I am for the precious cargo it contains, being the parent of a child who finds it hard to tell me about his life. This worn book contains all our lives. The small victories and challenges, the progress made, thwarted, then remade; the triumphs of communication, social interaction; school trips achieved (I can’t believe you got him on that bus!); new foods tried, new words spoken, the sudden voracious reading; and above all, every single day, the unwavering commitment to meet the needs of our child. To understand him, help him, celebrate him. I think of all our careful words ferrying back and forth across Edinburgh, transported by one of the nine boys with additional needs, to your class. The one who belongs to me. My brilliant, exuberant, autistic, six-year-old son.

It won’t surprise you to hear that it was one of the most difficult decisions of our lives, deciding whether he would be better off in a mainstream or specialist setting. Cuts in funding for pupils with special educational needs have been brutal, as we all know, and devastating for families like ours. In another, kinder, time we probably would have opted for mainstream because I believe in inclusion and know my son could thrive in the local primary school … with the right support. In the time in which we all find ourselves, however, we didn’t want to see if he would manage. We wanted him to be happy. So we applied for specialist provision.

Well, we hit the jackpot. My son is now a pupil in his second year of a specially tailored language class where he is following the national curriculum at his own pace, in his own idiosyncratic (often mysterious) way. Not a day goes by when I’m not grateful that my son is one of your pupils. You, an ex-speech and language therapist and teacher fresh out of training and on your first job, who he talks about all the time. You, who we recently found out is soon leaving the school.

The change will be hard for all of us, particularly my son. Already he is talking about you being “at Edinburgh Waverley”, which, as you know of our train-obsessed boy, is where he often imaginatively sends people when they say goodbye. To his favourite place on earth. The station.

We miss you already, Emma and we thank you. Edinburgh Waverley is lucky to have you.

Chitra

 
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schizopath

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I have high functioning autism and I absolutely get euphoria from MDMA but what it also does it makes me more social and emotional and open with those emotions. Which I guess is what it does for everyone, nothing special, except I normally feel emotionally numb and unable to connect to anyone and MDMA just brings up all these feelings in me that are usually just not there. I've been able to open up and express things I couldn't even put into words before.
Same here. I once went to a drug therapy/drivers lisence testing meeting on mdma and finally said and acted the way I only wanted to earlier.
 

Painful One

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@mr peabody
Could you do one of these on Narcolepsy and the use of GHB?
Apparently, the cataplexy is triggered by Strong Emotion.

Let me know if you do. I need help.
Thank you!
 

MountainTrails

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Wilson Wilson's comments on emotional accessibility had me nodding. I have genuinely struggled to understand and explain what the hell seems to be going on for me with MDMA, but have come up with the phrase "I get emotional processing" (I can access and process emotions to an unusual degree, for me) as a reasonable start. I don't really understand it, but there it is.

The lack of euphoria/well-being in my case isn't so easy to figure out -- there are too many possibilities that I can't disambiguate away. I'll probably lay it all out in a post and see what people think. But still, that was what got my initial attention reading anonymous autistic trip/experience reports floating around the Internet. My experiences across the universe of substances and time have mostly been very typical and what might be expected, FWIW.
 

mr peabody

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@mr peabody
Could you do one of these on Narcolepsy and the use of GHB?
Apparently, the cataplexy is triggered by Strong Emotion.

Let me know if you do. I need help.
Thank you!
GHB for narcolepsy in adults*

Xiao-Min Xu, You-Dong Wei, Yang Liu, Zuo-Xiao Li

Gamma hydroxybutyrate (GHB) is a chemical found in the brain and other areas of the body. It can also be made in a laboratory.

GHB used to be available as a dietary supplement in the U.S., but it was taken off the market in 1990 because of safety concerns. GHB and two closely related chemicals, gamma butyrolactone (GBL) and butanediol (BD), were linked to 3 deaths and 122 serious side effects. Nevertheless, secret production and sales of GHB continued, often on the Internet.

Continued interest in GHB might have been fueled by GHB's reputation as a "date rape" drug. Under the Date-Rape Drug Prohibition Act of 2000, regulation tightened. GHB was classified as a Schedule I controlled substance, like heroin. It is now illegal for Americans to produce, sell, or possess GHB except for medical use. A prescription form of GHB remains available, but the only legal access to this drug is through a physician or other healthcare provider who is licensed to prescribe medications.

GHB is used for depression, weight loss, muscle building, and relief of some fibromyalgia symptoms including pain, fatigue, and sleep problems. It is also used as an alternative to the dietary supplement L-tryptophan for promoting relaxation and sleepiness. People who are addicted to alcohol or narcotic drugs sometimes use GHB to help them manage withdrawal symptoms. It is also used to cause sexual arousal.

The prescription form of GHB has been approved by the U.S. Food and Drug Administration (FDA) for treatment of narcolepsy, a sleep disorder caused by the brain's inability to regulate sleep-wake cycles. People with narcolepsy experience irresistible bouts of daytime sleep. They can also experience muscle control problems, paralysis, and hallucinations. GHB is available under the generic name sodium oxybate and trade name Xyrem (Orphan Medical) for the treatment of paralysis associated with narcolepsy. It is a Schedule III Controlled Substance, which means extra paperwork is necessary when this drug is prescribed, and prescriptions for this drug receive special scrutiny from regulators.

Health care providers use GHB intravenously to numb pain and reduce pressure inside the head after a head injury.

How does it work?

The natural function of GHB in the body might be to slow down brain activity during sleep. GHB affects several nerve pathways in the brain, including activating the body's pain-killing (opioid) system and raising levels of growth hormone.

- GHB was effective in adults with narcolepsy and its effects on many aspects of narcolepsy were dose- and/or time-related.
- Only treatment with 9 g/night GHB resulted in a significant reduction of both cataplexy and objective daytime sleepiness.
- The greatest reduction in cataplexy achieved at 4 weeks of 9 g/night GHB treatment.
- GHB was less well tolerated than placebo because of dose-dependent side effects.

Occasional patients may find that regular napping is sufficient, but most require medications that reduce sleepiness and cataplexy.

Napping and sleep hygiene — One or two well-timed, 20-minute naps will often improve sleepiness though some patients only benefit from long naps. Specifically, a short nap around 1 or 2 PM is often helpful as it can improve alertness for one to three hours, reducing the need for stimulants in the afternoon. If it can be arranged, a brief nap at work or school is often helpful.

Conclusions

GHB was effective in improving narcolepsy-cataplexy and related symptoms in adults, but less well tolerated than placebo because of dose-dependent side effects.

*From the articles here:

 
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