Help, I Need Somebody (But Since I'm the Mom, the Answer Is No?)

A Kansas single mom of a severely autistic son discovers that the desperately needed supports denied to her are readily available to foster carers. Another tale from our broken system.

The author’s son enjoying a birthday outing.

By Beneeta Dean-Felton

I am the proud mother to three beloved sons, the middle of whom has a severe form of autism. At 12 years old, Preston is nonverbal, is not potty trained, and already has the size and strength of a man, which is a problem because he can be aggressive. If he pushes you, you can’t stop him and if he runs away, you might not catch him.

A few years ago I moved from New Hampshire, where I had been teaching, to pursue a new teaching opportunity at the federal penitentiary in Leavenworth, Kansas. Of course I needed help at home, particularly before and after school when I needed to be at work and couldn’t physically be there for Preston. In Kansas, disability services are determined by the county. As it turned out, my area had the worst services in Kansas. Everything is contracted out, a decentralized system so complex it felt like a corn maze where you can’t find the end: calls that were not returned, year-long waiting lists, and already-full agencies. I have a three-page document that shows every single service I asked for and couldn’t obtain.

After pleading, the county office offered Medicaid and a before- and after- care assistant, contingent on my finding my own worker at $9.35 per hour, that would be paid through state Medicaid funds. I used every resource I could think of to find a worker: Facebook, Indeed, flyers and advertisement, you name it. I scheduled dozens of interviews. If I scheduled 30 interviews though, only about five people would show up. I did end up hiring two separate workers and in each case they worked one day and then quit. Working with a large aggressive child, really now a young man, was just too hard for $9.35 per hour.

I was then informed by our Medicaid insurer that if I didn’t try harder to find somebody they would take services away. They recommended an agency, but the first worker the agency sent quit after one day. Finally they sent a worker who stayed for three months. But the agency paid her late and their checks bounced, and she left as well. My employer reprimanded me for arriving late and leaving early from work, but I had no choice. I was then assigned to a job with strict hours and no access to my cell phone. The unbearable stress of my home and work situations took a huge toll on my mental and physical health. I asked the child welfare officer what else they could offer me. The answer was “There is nothing I can offer you.”

At one point I made the difficult but desperate decision to leave Preston at home in the care of his older brother who would put him on the school bus. Unfortunately, my eldest fell asleep and Preston eloped, ending up in the street naked (he hates clothes so much). I am obviously not proud of this episode and regret what happened, but in my experience almost every family with a severely autistic child experiences something very similar to this. The police took him to the hospital, and the Department of Child and Family Services asked if I wanted to put him in foster care. At that point that was my only option to get him services. Preston has now been in state custody in a foster home since November 2018. Even though this is not a case of abuse (instead, Preston is deemed a “child in need of care”), I am treated like a felon, allowed only weekly, one-hour supervised visits with him. 

During a case plan meeting, the foster home provider said she needed an array of services to care for Preston, including aide support, respite, and home therapy. And guess what, she got them. Wait a minute, I said, what do you mean she instantly gets these services I’ve been fighting to get for years now? The response? I’m not entitled because I’m the biological parent. 

This was complete lunacy. It seemed the state of Kansas would rather separate families, at incalculable emotional not to mention monetary expense, than offer needed support in the first place. It was a perverse penny-wise-pound-foolish situation. It also occurred to me that if I had moved just 20 miles away, to Missouri, I would not be in this predicament, we likely would have received appropriate services in the first place. Autism is like a game of lottery, you luck out or you don’t. And if you don’t your life can become a living hell.

Through this painful process my income was too high to get a court-appointed lawyer and I can’t afford a private lawyer. The judge in this case recognized the injustice of my situation and appointed me a lawyer. I am now working with him to figure out next steps. The best thing for Preston may be placement in a full-time residential school where he can have access to vocational services, social opportunities, a vocational farm, therapies and so much more than a foster home could. But he could also return home. If only I could get the help.

Beneeta Dean-Felton is the mother of three boys, one of whom has a severe form of autism. She lives in Leavenworth, Kansas.

The Crisis Call No One Is Willing to Hear

A family’s trip through “the worst hellish nightmare you could ever have” and a system unprepared and unwilling to help.

The author, right, visiting with his son Joshua.

By Vance Goforth

We begged for years for help to no avail. This is the story of our son Josh, who we adopted after he suffered severe abuse in infancy, and who has severe nonverbal autism, along with comorbid conditions like seizure disorder, cerebral palsy, bipolar and disruptive mood dysregulation disorder. He is now 18 years old.

The behaviors started in childhood. By eight years old, issues at school got progressively worse and he was put on home bound after they became so severe the school system couldn’t keep him safe anymore. We sought help through doctors and medications at first and then psychiatrists who recommended inpatient treatment ASAP. He was even accepted into a treatment facility only to be called the day before admission to be told that they couldn’t treat Josh because we owned a wheelchair and their facility wasn’t ADA compliant. 

Everything started escalating during a trip to town a few years ago, Josh got upset and kicked out our van window and tried to crawl out at 55 miles per hour.  I had to pull him back into our van and tried to keep him calm until we could get home. We decided to call a help number on my insurance card and see what they recommended. To our shock, they didn’t know what to do, so they called the Department of Children’s Services. DCS told us since this wasn’t an abuse case, if we didn’t see them in 48 hours then they weren’t coming. So there we were, making calls that no one knew what to do with and ended with us facing crisis level behaviors with no help.  

The behaviors kept escalating and he was targeting our youngest daughter to the point that she was hiding daily from his outbursts. The nightmares really started as we began to call for help again. As we called crisis during these behaviors, we heard statements like, “We’re not prepared for a child as low functioning as your son,” or “If your son was suicidal then we could help.” Yet again, crisis responders would leave and we were dealing with the severe outbursts on our own. 

We were advised multiple times to take Josh and “drop him off” at an ER department and let the state take custody. We were also told to get a divorce, because “it’s easier to get help if the parents are separated.” Needless to say, we didn’t want to call crisis after some of the interactions we had. 

Finally, we kept begging for help and the Tennessee Department of Intellectual and Developmental Disabilities came to our home and told us they would find us help. DIDD couldn’t offer us anything until Josh turned 22, so they called and set up an appointment with Children’s Services. We were nervous about this because of the reaction we had before but we agreed to go to a meeting.  

During this interview, we were asked why Josh was no longer welcome in our home. I explained that wasn’t the case, we just needed help desperately. They requested documents from us and I provided them and we never heard back from them. Joshua’s behaviors had become daily at this point and after two weeks, I called DIDD and asked why they told DCS that Josh was no longer welcome in our home. They said, “You don’t understand, if we didn’t report it that way, they will never help your family.” I was absolutely blown away after this, not only did we not get help, they never followed up on the situation and he was getting worse by the day.  

DIDD finally made a referral for Joshua to get into a new state program called ECF choices in July 2016. He was accepted into this program and we were told he would get respite care, in-home services and other therapies and resources as needed. We thought yes! We’re finally getting help! But days turned into weeks and weeks into months. My wife was sending emails to our coordinator begging for help but the reoccurring theme was “no providers available.”

From 2016 to May 2017, the behaviors increased exponentially and had become very dangerous with severe aggression and self-injurious behaviors. In May of 2017, we still had not received the promised services and I was out of town for a conference when I received a call that Josh had a severe outburst and my wife had no choice but to call crisis again. This time crisis said that Josh needed help but couldn’t find any facilities that had open beds. He was extremely helpful but every path he tried was a dead end. 

So he called DCS, and this did not go well for the situation. They came out while crisis was still at our home and began interviewing our other children on our back deck as they watched through the window as my wife was hit, slapped and kicked just trying to keep Josh from hurting himself. The crisis worker ended up apologizing for calling them because he said “I’ve never had an experience like this before,” and he couldn’t understand why the situation was being handled the way it was.   

The social workers “watched through the window as my wife was hit, slapped and kicked just trying to keep Josh from hurting himself.”

After all of this, my wife and family were left alone with no help after he got his meds and took a nap. The next day our coordinator said to meet her at a Knoxville hospital and they would get Josh treatment. My wife and father had to self-transport Josh even though we had voiced concerns about severe outbursts he had while we were driving. When they arrived, we were yet again turned away and told that the hospital couldn’t provide treatment. Even though they would not treat Josh, they didn’t want my wife to leave with him over safety concerns. They also advised taking him to an ER and discussed relinquishing custody in order to get help.  

Finally, they got Josh home and he was accepted to a hospital in Georgia the next day. Again, my family had to transport him because an ambulance service refused to do the transport due to his aggressive behaviors. He spent 12 days at this hospital and was sent home because “they witnessed no behaviors.” Four days later he was tearing our house apart and hurting himself severely. I made the call to get him back into the hospital but was informed, “it doesn’t work that way.” I was told he had to be turned down by every treatment facility in Tennessee, again. This process takes months and he was getting dangerously aggressive at this point.  

We were provided with ABA therapy at this point and it didn’t take long for our therapist to see that Josh needed residential treatment and that was what they recommended. Our therapist eventually resigned and we didn’t get ABA after that. We finally received one-third of the in-home services that he was supposed to get in September 2017 and the behaviors kept increasing over the next few months. He had got so severe that he had broken several teeth and had done over $17,000 worth of damage to our home and vehicles.

My wife and I had become increasingly isolated from everyone around us during this time and we struggled to keep everyone from seeing how severe our son’s behaviors had become. We basically had confined ourselves in our home, taking turns trying to minimize the behaviors as much as we could all while being told that help is on the way.   

I cannot even start to describe what life was like during December 2017 through February 12, 2018. The behaviors had reached a level that can only be described as the worst hellish nightmare you could ever have. To watch your child you love so much inflict so much harm upon himself is too much to bear. The strain this brings is indescribable and even that isn’t an accurate description.  

“To watch your child you love so much inflict so much harm upon himself is too much to bear. “

The stress was building day by day and on February 2, 2018, the nightmares went into overdrive. We were coping the best we could and trying to keep life as semi-normal as we could for our other four children. On that day, my wife Kristy had stayed with Josh while I took our other son Camden to workouts. I was on my way home when I received the phone call. At first the call was totally indistinguishable from all the screaming that was taking place. My heart sank as I tried desperately to find out what was happening, then I figured out it was one of my daughters that had called and finally I heard “It’s Josh” through the screams.  

It felt like a shock of electricity went through me before I went completely numb. I had no idea what was going on but I was trying desperately to just get home. I was crying and praying as I drove as fast as I could and Camden was crying hysterically and begging God to help his brother. I actually arrived before the first responders and as I ran in the house, Josh had just stopped having the most severe seizure we had ever witnessed. Kristy had called 911 when the seizure kept going to the point that Josh quit breathing and turned blue. He gasped for air and started breathing again just seconds before I arrived home.  

Whatever happened during this seizure changed Josh and the behaviors became even more amplified than before. Over the next ten days, I can’t even say we were handling the outbursts because that would be a lie. The behaviors reached a fever pitch that ended with extensive injuries to myself and Josh. 

“The behaviors reached a fever pitch that ended with extensive injuries to myself and Josh.” Here, two photos of the author after a series of his son’s aggressions.

Josh would bite his wrist until it was almost down to bone and began breaking all of his teeth off by hitting his head on the floor and walls, and hitting his hand while biting it. I was bitten over 50 times during three different outbursts and received lacerations, bruises and a severe black eye that may have caused permanent damage. Josh had extensive injuries from the self-injurious behaviors and was not calming down at all. We visited two different ER departments during these outbursts and mobile crisis was contacted twice. Mobile crisis never did the face to face evaluation that is required by state guidelines. 

We took Josh back to his doctor the next morning after being in ER rooms all night and his doctor forced the issue and made crisis respond. Josh was eventually transferred after a three-day stay in another ER room but we had to get lawyers and judges involved just to get the treatment he needed. After a few weeks and multiple legal issues he was transferred from Georgia, where they had said before he wasn’t having issues, to South Carolina where they recognized the severity of the behaviors. He has been in treatment there for 14 months now. 

Joshua is making improvements in his residential program. It took many years of traumatic dead ends before he received appropriate treatment.

When Josh finally received the needed treatment, he started slowly making progress. Springbrook has been amazing and not only treated our son but also encouraged and gave advice to the whole family. After 14 months of treatment, Josh is scheduled to be the first resident in a new experimental housing program in Tennessee. Hopefully he will be ready for this program within the next month or two.

Without naming organizations specifically, here are just a few things we have been told while seeking help for Joshua.

1) If your son was suicidal we could help, but since he is so low functioning we are unprepared for a child like Joshua.

2) Your best option may be to drop your son off at a emergency room. (Basically telling us to abandon him! Yes, this was really suggested to us and more than once!)

3) You’re approved for certain services but they aren’t available in your area.

4) Your behavior analyst quit and you will not have these services anymore because one isn’t available in your area now.

5) You can’t get the services you are requesting because your son is a minor.

6) You are approved for respite care but it’s not available to minors.

7) Your son can’t go into residential care because he is a minor.

8 ) You have 24 hours to pick up your son or you will be charged with abandonment. While another agency is telling you he can’t return home until he is treated and is stable.

9) Every facility in the state must deny admission for your son before you are eligible.

10) We can’t take your son because our facility is not ADA compliant.

11) We can’t take your son because this is not an abuse case.

12) If we separate or get divorced we might get priority for services for our son.

And the list goes on. Is everyone seeing the need for changes to the system yet? —VG

We were in pure survival mode for so long, we didn’t know how much all of this had affected our other children and family members. Joshua’s siblings love him dearly and were quietly trying to deal with the situation as they watched things that no child should have to ever witness. After Josh was in treatment a few weeks, they began to open up to us about everything and it hit us like a ton of bricks. We were so consumed by managing the behaviors and keeping everyone safe, that we didn’t realize how much the stress was affecting all of us. Slowly but surely, the kids began to heal from all of the trauma and we started seeing improvement in school and other activities.

After Josh finally got the treatment he needed, we created a Facebook page, A Voice for Joshua. I was determined that I would advocate for issues affecting individuals like Josh who have severe ASD and comorbid conditions. I’m not the most eloquent speaker and my posts are usually more solutions-oriented than other bloggers who can effectively pull on heartstrings, but I’m determined to keep advocating and sharing his story until needed changes take place.  

Please join us in this journey and advocate for Josh and others who face desperate situations without appropriate resources and services.

Vance Goforth is the father of five who lives in Tennessee. You can find A Voice for Joshua at facebook.com/pg/changeforjosh

Autism's Quiet Heroes: The Siblings

Photo of Zoe courtesy of the author

By Melissa Collins-Porter

For this year’s autism awareness month, I’d like to honor and celebrate the siblings. They love their brothers or sisters fiercely, yet quietly endure being dragged to therapists’ offices and doctor appointments, become basically ABA-certified by the time they’re 12, and get used to only Mom or Dad coming to their events because one has to stay with their sibling. They often are forced to concentrate on homework amidst what reasonable people would call total chaos. From a young age, they have an awareness that at some point, they will likely become caregivers to their sibling. They may feel guilt about the fullness of their own lives (friends, sports, activities, travel, independence, college) in contrast to that of their sibling. They may feel pressure to be “the quiet one,” “the good one,” “the easy one.” They have become used to cancelled plans, destroyed or lost personal items, and giving up their own preferences to appease their brother or sister. They tirelessly stand up for their siblings when people ask questions, stare, or use “autistic” as a pejorative at school. Underestimate them at your peril, because they grow up to be extraordinary adults and you want them on your side. This one right here is my hero.

The writer is a filmmaker who lives in Southern California.

Federal Bill Would Put Jobs Out of Reach for Severely Autistic Adults

Everybody should have access to work, but a new bill, based on the fantasy that all intellectually disabled adults could achieve competitive employment, would trash cherished job programs for the severely disabled. 

Under the Transformation to Competitive Employment Act, the author’s 20 year-old severely autistic son, and countless others like him, will be relegated to the status of permanent volunteers, effectively prohibited from landing paid employment.

By Jill Escher

My son Jonathan is a delightful nonverbal autistic 20 year-old man. Powerfully built, he has a supercharged energy and a deep well of affection for loved ones and his iTunes library. But Jonny is also profoundly intellectually impaired. Accomplishing even simple tasks requires vigorous prompting and continuous oversight, and chances are that along the way he might bite, stand on, or even throw his chair. As muscular and lovable though he may be, his chances of landing a competitive job are exactly zero.

The TCEA was introduced on January 29, 2019 by Congressman Bobby Scott (D-VA-3), chairman of the House Education and Labor Committee, Senator Bob Casey (D-PA), and Rep. Cathy McMorris Rodgers (R-WA-5).

Nevertheless I can envision that some day Jonny could participate in a disability program engaging in simple but important work (albeit with hawk-like oversight and prompting), perhaps boxing or moving heavy objects, or picking up garbage. But under a federal bill introduced in January, Jonny’s hope for future wage-earning would be thoroughly trashed. 

The Transformation to Competitive Employment Act (TCEA) (S. 260 and H.R. 873) would, over a period of six years, completely phase out disability-specific sub-minimum wage programs, even those serving the severely cognitively disabled who would otherwise be unable to access work. The bill would also provide a grant program to help expand capacity for those capable of achieving competitive employment.

Listen, the TCEA is in part addressing an important issue. Section 14(c) of the Fair Labor Standards Act, which authorizes employers to pay specially tailored wages to employees with disabilities in certain restricted circumstances, has at times been abused by bad-apple employers to pay disabled employees less than they were worth. Though affecting a small portion of the 14(c) programs, the exploitation was indeed something to be remedied. The TCEA offers some needed fixes to our labor system by ensuring these workers have a way to move out of 14(c)  programs and into competitive integrated employment. Amen to this wage justice.

But for the more impaired portion of the disability community, the 14(c) program fills an urgent need. It is simply inconceivable that a commercial employer would willingly hire someone like Jonny, who cannot talk, read, or write, and at best can follow only one-step directions, over a non disabled person whose productivity is ten times greater and who is unlikely to chew the furniture.

Some disability advocates are telling lawmakers that all people no matter how disabled can find integrated, competitive employment. Please. Just stop. I don’t know what these advocates have been smoking to spout such fantasies, but clearly they are not spending much time with guys like mine, nor have they ever tried to employ them.

So it should be clear to any fair-minded person that the TCEA risks throwing the jobs baby out with the social justice bathwater. Beyond its preposterous assumption that all disabilities are created equal, let’s look at some other problems with the bill: 

In addition to the TCEA, the Raise the Wage Act, H.R. 582 and S.150, also contains provisions to close 14(c) options. It is also sponsored by Bobby Scott (D-VA). This bill is tied to the movement to raise the federal minimum wage, so it has many more sponsors (currently 204, versus 20 for the TCEA).

• The TCEA ignores the staggering increase in severe autism and what should be a clear imperative to create vastly more, not fewer, options for day programing and supported forms of employment. In California, the population of adults with developmental disability type of autism will grow nearly five-fold over the next 20 years. Only a small portion of these adults can achieve competitive employment. The rest? We need to maximize their options, including work that pays special wages based on less-than-competitive productivity. 

• The TCEA dodges the obvious fact that subminimum wage work is but one benefit accruing to the significantly disabled clients. Work programs serving adults with significant intellectual disabilities like Jonny are typically run by mission-driven, not profit-driven, nonprofit organizations. These adults are typically also beneficiaries of supervision, therapeutic care, training, and social and recreational programs funded and provided by the nonprofits. It can be very costly to serve these disabled individuals: they often require high staff ratios, intensive supervision, crisis intervention and ongoing coaching. A standard job supervisor is unlikely to treat seizures, change diapers, or handle getting punched or scratched, to put it mildly. The extremely valuable, though non-monetary, therapeutic dimensions should be considered before over-simplistically labeling subminimum wages as discriminatory.

• 14(c) programs serving the significantly intellectually disabled provide a protected form of employment unavailable in the free market. “It’s not an employer-employee relationship,” explains Tracey Brown-May, Director of Advocacy, Board, and Government Relations at Opportunity Village in Las Vegas. “People employed here who are earning 14(c) wages are not at risk of being fired.” In other words, the employee’s needs comes first, and profitability is not the prime endpoint. The nonprofit work is typically tailored to the particular skillset of the worker, a customization unavailable in the free labor market where individuals are expected to conform to pre-established performance standards. Disability advocates often accuse 14(c) wage program of exploiting or abusing their disabled workers, but at least for severely challenged adults, the opposite is almost always true— the programs often protect clients from exploitation and abuse by offering a protected form of employment.

• No person with a disability is forced into 14(c) work, and wages are set carefully. The provision authorizes employers to pay specially tailored wages to employees with disabilities only when the employer can demonstrate, through an exacting certification process, that the worker’s productivity is compromised by the disability. The certification requires a careful calculation of fair wages based on productivity and continuous re-evaluation of the employee’s capacities to ensure wages keep pace with skills. And of course the worker would also need to agree to the wage. Programs must be re-certified every two years by the Department of Labor, which has the duty to identify and remedy any abuse or exploitation it finds during its reviews. 

• Most workers with disabilities, for example physical disabilities, are already in the competitive market. Retaining a 14(c) option does nothing to negate or undermine expansion of competitive employment for those capable of that option. Both work options can and should peacefully coexist to serve a dramatically diverse disability population. As Harris Capps, the father Matthew, who loves his job in a Ohio work center, asked, "Why do higher functioning disabled persons and their lobbying organizations want to deny lower functioning persons, the right to work? If a higher functioning individual is able to get a job providing a mandated minimum wage, surely, they already have the minimum wage law in effect to protect them.”

Loves his job: Matthew Capps loves nothing more than to report for work. But the TCEA is putting his job, and thousands of others, at risk.

• Not supported by data. Data from states that have closed their sheltered workshops do not necessarily demonstrate a correlated increase in competitive, minimum-wage employment. In Maine, two-thirds of former workshop participants are now unemployed. Those adults with I/DD who do have jobs work only an average of twelve hours a week, which is the lowest average in the country. In Washington state, more than 80% of those with severe cognitive impairments remain unemployed. Vermont reports fewer adults with I/DD in supported employment since closing its sheltered workshops in 2002. In short, when sheltered workshops close, participants often end up idle at home, lonely and unemployed, or if they work at all, with decreased job hours and decreased total wages. The other alternative — volunteer work in the community — can sometimes provide community, engagement and pride, but in reality, volunteering for commercial employers often suffers the same challenge as competitive employment: that option does not offer the support needed.

Every family affected by severe autism should know about the TCEA and oppose it in its current form. While federal policy should certainly promote opportunities for competitive employment when possible, guess what — our pizza can have both pepperoni and mushrooms. Let’s expand capacity for competitive wages using the planned federal grants, while also retaining vital options for our severely disabled loved ones.

As Opportunity Village’s Brown-May says, if 14(c) is phased out, “employment opportunities will go away for people with a very significant level of disability. They are the people who will get hurt.”

Jill Escher is President of the National Council on Severe Autism, President of Autism Society San Francisco Bay Area, and founder of the Escher Fund for Autism. She is the mother of two children disabled by nonverbal forms of autism.

See NCSA Position Statement on Vocational Options: ncsautism.org/vocational-options

A Federal Policy Victory for Adults with Autism

A 2014 Medicaid guidance, now withdrawn, had the effect of substantially restricting program and residential choices for autistic adults precisely at a time of surging need for new options.

Amy Lutz, now NCSA’s secretary, discussed the problems with the former Medicaid guidance in the article, Who Decides Where Autistic Adults Live? published in The Atlantic.

We are pleased to inform you of a significant policy victory for adults with autism.

The surging population of young adults disabled by autism is creating unprecedented demand for a wide spectrum of supportive programs and residential options across all our communities. 

NCSA will update this page soon with more details about the CMS guidance.

Together for Choice press release here

Many of these options will be funded in part through federal “Medicaid HCBS waiver” dollars. This is federal money designed to subsidize services in one’s own home or one’s own community, and outside of state institutions.

In 2014, Medicaid’s administrators, the Center for Medicare & Medicaid Services (CMS), surprised the developmental disability community by issuing a sub-regulatory guidance that has had the effect of substantially restricting program and residential options for adults with autism and other DDs. The guidance targeted farmsteads, disability-specific communities, residential schools, campus models and other intentional communities as “isolating,” and therefore presumptively noncompliant with the CMS regulations, a presumption that could be overcome only after an opaque process called “heightened scrutiny.”

Fortunately for our community, this past Friday CMS issued new HCBS guidance which supersedes the previous guidance. You can view the new policy here, which is written in FAQ form. Advocates spoke with CMS staff on Friday and confirmed the following:

• Settings described in previous guidance are no longer presumed institutional nor isolating and will no longer be forced to go through heightened scrutiny if the state determines the setting is compliant with the HCBS Final Rule.

• Consumer-controlled settings are presumed compliant.

• Settings previously submitted for heightened scrutiny may no longer need to go through the heightened scrutiny process if the state determines it is compliant or can become compliant by July 2020.

• The role of an individual’s person-centered plan is paramount in guiding services, their home preferences, and access to the greater community.

• The new guidance is outcome-oriented and focuses on the setting’s facilitation of community engagement as described in one’s person-centered plan.

This welcome development will help our community mobilize as many options as possible for our burgeoning and incredibly diverse population disabled with autism. We will update this page soon with additional information, but in the meantime for background information please see:

Visit togetherforchoice.org

Visit coalitionforcommunitychoice.org

• “Learn about the Issues” from Coalition for Community Choice

• Together for Choice website

• "Who Decides Where Autistic Adults Live?" by Amy Lutz, NCSA secretary 

• “The Federal Government’s Quiet War Against Adults with Autism” by Jill Escher, NCSA president

•  “You Can Choose Where You Want to Live... Unless You Have Autism" by Jill Escher. 
  
  NCSA thanks all the autism and disability advocates who pressed for common sense, person-centered policy changes, and who fought draconian rules that would have privileged a segment of the disability community at the expense of others, particularly those in need of strong supports. 

Sensory overload, water stims and tantrums: Autism moments captured in poetry

This evocative poetry, capturing moments familiar to many autism families, ping pongs its perspective, shifting from mother to autistic child, almost as if the duo were a single entity.

Writer Tom Graham is a 38 year-old autistic man who spent most of his school years in special education, diagnosed with a speech and language disorder/learning disability, before being re-diagnosed with Autism Spectrum Disorder. He spent five years of his adult life as a psychiatric inpatient and currently resides in supported accommodation in the southwest of England. We hope you enjoy his work. —The editors

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Enigma

Soulful eyes that rarely connect
nevertheless acutely aware.
A tangled mop of curly brown hair
grooming is so unfair.

Running in circles
a hand raised
fingers splayed
in front of the eyes.

The purpose of which
one can only guess
to make it less
filtering out the mess.

#Autistic

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Brotherhood

If it happens to be wet
your interest is a safe bet
it starts as a trickle
soon I'll be in a pickle.

Do I get in your way
or let you play
Mother will be cross
it's her loss.

Witnessing your joy
it's worth the ploy
as the taps run
it's all good fun.

Keeping a lookout
while you scream and shout
the floor’s a lake
you're killing me, Jake.

Scrambling for the mop
that's your lot
you're bound to resist
she's gonna be pissed.

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Overload

A hand to the mouth
it's all gone south
he takes a bite
trying to set things right.

Chewing his flesh
making a horrible mess
it's a cry for help
he's ready to melt.

A trickle of blood
becomes a flood
it’s gone too far
there’ll be a scar.

Time to intervene
makes me feel mean
he begins to scream
it's like a bad dream.

Trying to get a grip
everything’s gone to shit
love will out
that's what it's all about.

Tom can be contacted via his Twitter account, @serverusautismo.

All poems ©2019 Tom Graham

I’m 80 Years Old and There’s No Post-Mom Transition Plan for My Severely Autistic Son

Medicaid waivers are a godsend for many autistic adults, but who oversees complex care after a parent dies?

By Martha Moyer

I am 80 years old and have a son, Seth, age 45 who has severe autism. I was one of the first in Texas to have advocated for the Medicaid Home and Community Based Services (HCBS) waiver which has given him the opportunity to receive care in his own apartment, where he has lived since age 22. The HCBS waiver is a lifesaver for my son, because before that, federal money would only pay for care in a state institution.

Seth has autism, intellectual disability, mental health issues, OCD, and paralyzed bowels due to neglect he received in an institution. He also has minimal language ability. He stands over six feet tall and weighs 240 pounds, is quite unstable and has been in two mental hospitals in the past. When he gets angry he swings at anything in view including pictures, he breaks glasses and even throws furniture, which means no fancy house decorations for me because he comes home on two weekends a month. Being so volatile also means his own home has few decorations. But thanks to his caregiver Seth goes out in the community daily and goes to special events such as dances and parties for the disabled.  

When we arrived in Texas around 1982, the funding for I/DD services outside of state institutions was minimal. But when news about my son got in the newspaper telling about his violence, he was granted state residential care funds. Shortly after, he ended up in a private institution here in San Antonio funded by the school district. I could not risk having my son lose the state funds, so I had the commissioner set aside the funds for when he aged out of the program. After we secured funding for his own apartment, the state used the funds to supplement HCBS federal money to pay for the support services. 

While HCBS has been a godsend in many ways we need to be honest and acknowledge that HCBS is not set up for complex individuals like Seth.

The biggest problem is that while he should not live in a state institution, he still needs a comprehensive approach to care. You can’t just put him in an apartment with a caregiver. Someone needs to set up and manage all parts of his program — the person-centered plan and quarterly review of services, finding and maintaining and paying for housing, including Section 8 funds, doing the staffing and training and regular supervision, behavior management, and dealing with medical needs, bookkeeping and payroll — and then continuously manage all these moving parts and all the paperwork.

While I’m alive and functioning I am the program administrator. And an 80 year-old friend volunteers to do the billing. I can’t say enough for my friend’s generosity, but I doubt anyone will take our places for free. 

The second big problem is crisis intervention. For example, last night the city water company was working on fixing a leak so they shut off all water to the building where my son lives. Like so many people with autism he went into a great meltdown because water flowing through his hands is his thrill. He tried to kick the caregiver, destroyed many of his items, and couldn’t be calmed. The caregiver had to call the police, who took over an hour to get there, and when they did appear they took him down to the police car to give the caregiver a break. The water didn’t come on so they took him to a psychiatric hospital and dumped him there. When an adult with severe autism has a meltdown it shouldn’t come to this, but HCBS is fragmented without the on-call help that is often needed.

A third issue with HCBS is that costs for complex medical care are not covered. My son needs a procedure called the PIE, pulsated irrigated evacuation system, that keeps him alive. His bowels are paralyzed and nothing will make them work. I can’t get this procedure covered by any of his services including Medicaid because there is no code for it. We pay over $500 a month out of other funds for the PIE supplies.

One bright spot is our use of what is called a Microboard, which is basically a very small corporation set up to provide care and funding for a disabled person. When I am not around anymore my son’s microboard can help see that my son is not “thrown away” and that he receives proper care. 

But at 80 years old I worry about what will happen to my son when I die. The alternative to HCBS is either a state institution or group home which I fear would kill him. His needs are such that none of the group homes would want him. The amount for the PIE is one big reason no group home wants to care for him. Group homes also don’t want to deal with the violence.

I am fearful about re-institutionalization because I have a friend whose violent son with autism ended up in an institution and staff beat him until he never walked again and ended up in a vegetative state. She had to fight for the state to allow her to sue. Texas legislators told her she couldn’t sue because the state had sovereign immunity. She was finally compensated.

My point is that the HCBS program needs to be developed to address the complicated needs of adults with severe autism. We need package programs offering a lot more supervision and management than is currently possible. The system is very fragmented and depends on parent managers. And we have an expiration date. And parents never know an expiration time. And in some cases there are no relatives left or able to help.

— Martha Moyer lives in San Antonio, Texas.

[Editor’s note: Medicaid HCBS waivers are implemented differently in each state, and some issues discussed in this blogpost are specific to Texas. Texas is also home to the longest HCBS waiver waitlist in the country, with more than 150,000 people awaiting waiver services.]

For Our Children with Severe Autism, Speak Loud, Speak Proud

By Kim McCafferty

A couple of weeks ago while procrastinating from what I should have been doing and scrolling through Facebook I saw a post that immediately caught my interest. It was from the National Council on Severe Autism (NCSA) which I had never heard of, and the title read “Suffering in Silence: The Dark Side of Autism.”

I actually put down my chocolate for better scrolling access, and I never put down my chocolate for anything.

I read the article by a mom out in California who spoke about an incident she had lived through with her eleven-year-old severely autistic son, one which culminated in the California Highway patrol pulling up behind her as she parked her car on the highway and hoped to quell the rage her son was displaying toward her so she could safely leave. Both her love and fear for her son came through in every sentence, as well as her heartache in knowing that an attempt to take him ice skating could end this way.

I personally have a 15 year-old severely autistic son with accompanying OCD, tics, and intellectual disability. Justin and I have a profound connection — this is a child who kisses me even when he doesn’t want anything and hugs me on a frequent basis. We have a bond that through insomnia, aggression, refusing to eat, soul-sucking OCD, and last year also a terrible movement disorder, has remained true and strong.

I write a blog about him, Autism Mommy-Therapist, because I want the world to see him as I do, a kind-hearted, intrinsically happy almost-man, despite his challenges. And yet I also share about his incidents of aggression, the fear I’ve felt when dealing with my son’s meltdowns, my anxiety for his future. I do this in part so that some other parent out there going through this will not feel so alone. I also do this for my own mental health, because it’s important that I have an outlet to share my experiences with my severely autistic child.

And I do this in the hopes that more parents will share their stories, and this underserved segment of the autistic population will finally get the attention, and the services, they deserve.

“And I do this in the hopes that more parents will share their stories,
and this underserved segment of the autistic population
will finally get the attention, and the services, they deserve.”

Stories of high-functioning autistic children and adults are easy to find. As the mother of a twelve-year-old on that end of the spectrum I want him represented too. However my eldest son is nothing like the protagonist on “The Good Doctor,” yet he also deserves to have his story told as well. The public badly needs exposure to this segment of the autism population, the one that nobody writes the “feel-good” stories about. The one that makes some of us uncomfortable. The one that will never star in a television series.

Autism acceptance is not just for the high functioning. Those of us with children and adult children on the more severe end of the spectrum need to tell their stories and have them be heard. Many of our children are silenced by the inability to speak or communicate through a device.

Their realities should not be silenced too.

I am thrilled with the creation of the NCSA. This is a platform for families with severe autism to finally have a strong voice. I am actively for any organization which can help my kids, and hopefully with time we will see NCSA as a major contributor to the goal of realizing safe, happy and productive lives for those severely affected.

Kim McCafferty is the mother of two sons with autism. She lives in New Jersey.

“Hit Me With Your Best Shot”: A Story of Severe Autism on Public Radio

In a rebroadcast of This American Life airing beginning this Friday, Chicago-based writer and psychologist David Royko and his wife Karen discuss the decision they faced to place their severely autistic son in a residential facility. Excerpt: “On a typical day our son Ben empties the contents of cereal boxes and egg cartons onto the floor. He opens car doors while we’re driving. He walks into traffic. He throws himself up against the sliding glass door in our den…. He dwarfed everyone in the house but me, which is why my wife Karen’s arms are covered in bruises, scratches and scars….”

By David Royko

A pleasant/unpleasant surprise.…

I just got word from the radio program This American Life that they’ll be re-running our episode from 2007, “Hit Me With Your Best Shot” (it comes in the second half-hour of the show, "Unconditional Love"), centered around Ben's move from home into residential. Pleasant, because I never would have thought it would still be resonating so fully a dozen year later. Unpleasant, because I never would have thought it would still be resonating so fully a dozen year later. We STILL are far away from figuring this severe autism-thing out and how to treat it — effectively.

Anyway, it’ll be airing on Public Radio beginning this Friday. The funny thing about our modern age is that, as I was told some time back by Public Radio’s RadioLab when I asked them when an episode I participated in would be airing, they said, “Oh, sometime in the future. We don’t really pay attention to that – we get most of our listeners via the podcast.”

So, if you’re in my general demographic and still, um, “tune in” to terrestrial radio, there you go — this American Life is locatable on your local FM dial. But, truth is, anyone can hear it via podcast (see link), now and any time over the past dozen years. Man. Choices choices choices. It’s enough to make your head spin. Or mine anyway.

Listen in: https://www.thisamericanlife.org/317/unconditional-love/act-two-0. (19 minutes)

More from David

His blog:
Juggling Autism: The Chronicles of Ben Royko-Severe Autism in Real Time

His Huff Post blog:
Huffington Post: David Royko: Psychologist; Director of Family Mediation Services; Writer (autism, music, children of divorce); Ex-Drummer; Gluten-Eater.

“Quasi-Genetics” at the Roots of Autism?

Though it’s impossible to have a genetic epidemic in the classic sense, certain exposures to reproductive cells may quietly engender a quasi-genetic epidemic. The authors explain the science and suggest a new priority for autism research.

By La Donna Ford, MD, and Jill Escher

Answers regarding the causes of autism have been frustratingly elusive. Only a fraction of cases have been attributed to genetic mutations, and even fewer to fetal exposures. Despite decades of intensive research, the vast majority of autism cases remain head-scratchingly idiopathic, that is, without a known cause. 

So what hidden forces could be fueling the dramatic increase in prevalence, which has reached an alarming 1 in 59 children? And how could a disorder seen to be strongly heritable increase, at all?

In this article we explain the “quasi-genetic” hypothesis of autism, a relatively new concept that could help answer those questions. It could help explain autism’s heightened risk among siblings even in the absence of genetic causes (often called the “missing heritability” of autism), its swift increase in prevalence over the past three decades, even its skewed sex ratio, among other puzzles. You will see that while it’s impossible to have a “genetic epidemic” in the classic sense, it is indeed possible to suffer a quasi-genetic epidemic, given the right conditions.

“Glitches in these molecules can alter the way genes are expressed without changing the underlying genetic code.”

What do we mean by this quasi-genetic stuff? Aren’t all of our inborn traits genetic? Yes, we would say most are. But our egg and sperm (also called germ cells), highly specialized cells that are exquisitely and minutely programmed to enable the development of an entire human, are not merely sacks of DNA. They also harbor billions of molecules that help control how and when genes function — poised to turn them up or down, depending on the time and the tissue. Glitches in these molecules can alter the way genes are expressed without changing the underlying DNA code. In this way, even without a mutation, non-genetic glitches can derail normal development.

We realize this realm of science is unfamiliar to most folks. Certainly it appeared nowhere in our high school biology textbooks. But over the past decade or so it has become increasingly clear that these quasi-genetic factors help modulate development, and, moreover, that they can be vulnerable to a host of environmental factors.  

Egg (left) and sperm (right, as spermatogonia, the progenitors of sperm) contain the complex multi-layered molecular code for building a new human. Their heritable content is multi-layered and not limited to the DNA sequence. (Images from Embryology Education and Research website embryology.med.unsw.edu.au/embryology)

The quasi-genetic elements include the “epigenome” and “chromatin” of our cells. The epigenome essentially refers to the network of chemical compounds attaching to and surrounding DNA that modify genetic function. Chromatin basically refers to the DNA and its structural packaging which condenses and expands DNA in a way that helps regulate gene expression. These basic elements are fundamental to the differentiation and functioning of all our cells: while every cell features the same genome, these quasi-genetic forces help determine whether a cell becomes a brain cell or a skin cell, for example, and how those cells behave.

When toxicants cause glitches in the quasi-genetic machinery of our germ cells, the effects are seldom straightforward, and they may or may not disturb the development of offspring. The glitches could be repaired down the line, could be negligible, or could be considerable. They might differ according to underlying genomic difference, or a multitude of complex biochemical processes shifting over time. The same exposure can exert different effects in different stages in different people. But in the end, as we will discuss, research has linked exposure —> germ cell glitches —> offspring perturbation of brain/behavior owing to quasi-genetic mechanisms. In biology, germ cells are increasingly appreciated not just as storage vaults for DNA, but as dynamic biological entities that can be responsive and vulnerable to environmental cues. [Alert to biology buffs: we are not discussing “transgenerational” effects, those effects that persist in the absence of a direct germline exposure. Rather, for the purposes of this article we are solely concerned with direct germ cell exposure.]

Now it’s time for us to dive deeper into science and history to explain why, despite some we’ve-turned-over-every-stone malaise in the “genes” or “environment” world of autism research, there is an entire dimension of risk that has yet to be pursued. And we can’t think of a better place to start our journey than in anesthesia research lab in New York City, circa 1980.

Turndorf was concerned about how common volatile anesthetic gases affected brain function in exposed fetuses, and also the next generation.

Dr. Turndorf’s anesthesia-exposed mouse eggs

In the 1950s and 60s America experienced a chemical revolution — our fields clouded with new pesticides like DDT, clothing glowed with vibrant synthetic dyes, kitchens filled with Tupperware, and pharmacies brimmed with new synthetic drugs. In the field of anesthesia, brilliant chemists synthesized novel volatile anesthetic gases that helped keep patients sedated and inert during surgical procedures and were safer to use than their predecessors. Though utterly miraculous in enabling modern surgery, these powerful chemicals also had their downsides, among them possible neurological damage. 

In about 1980, Herman Turndorf, MD, Professor and Chairman of Anesthesiology at the New York University School of Medicine, and colleagues wanted to see what effect commonly used general anesthetic agents (“GA”) had on the learning and behavior of mice exposed in the womb. Translated to a real-world question, they sought to discover whether surgical anesthesia in a pregnant woman might cause brain impairment in her exposed child. Anesthesiologists like me (LDF) would of course want to know the long-term impacts of our sedation techniques, as would our patients. 

In a succinctly written 1981 paper, the team reported that the baby mice borne of gestating females exposed to two GA agents called halothane and enflurane suffered long-term learning impairment, performing poorly in food maze tests compared to control mice. This was not entirely unexpected. But, to our eyes, an additional finding stands out. 

The researchers did something remarkable in that they also looked at learning outcomes in six mice in the next generation. These mice were the grandpups of two females exposed to halothane as fetuses. These grandpups were just early-stage eggs, nested inside fetal ovaries of their fetal mothers, at the time of exposure.

An exposure to a pregnant woman can affect three generations: the mother, her fetus, and her fetus’s nascent germ cells.

Turndorf and colleagues seemed to understand that an exposure to a pregnant female can simultaneously affect three generations: the mother, her fetus, and her fetus’s germ cells. Because those germ cells are the delicate precursors to the gametes containing the fundamental blueprint for the next generation, contamination by a chemical or drug could therefore impair the grandchildren, born decades after the germ cell exposure.

“The grandpups’ impaired learning suggested the anesthetic agent may have caused a ‘genetic aberration’ in the exposed mothers’ fetal eggs.”

In their report, the researchers remarked on the outcomes of the grandpups borne of the exposed germ cells. It turns out they were found to be “significantly slower than control mice throughout the training” on all days of testing and all configurations of the maze. The researchers concluded that the grandpups’ impaired learning “suggests that the anesthetic agent may have caused a genetic aberration” in the exposed mothers’ fetal eggs (Chalon et al., 1981).

After this 1981 paper, Turndorf’s lab returned to this question of germ cell effects of general anesthesia in a different type of mouse experiment. Knowing that the GA agent enflurane caused damage to sperm (citing Land et al., 1981) and that halothane caused learning impairments in the generation borne of exposed eggs based on their own observations, the lab investigated the possibility that exposure of adult male mice to enflurane prior to mating could also affect the brain function of offspring, due to damage to the exposed sperm.

Once again, they found impaired learning function in the generation borne of the exposed germ cells, this time later-stage sperm instead of early-stage eggs. They remarked that it “seems likely that spermatogenetic changes, caused by enflurane, are associated with genetic alterations” that affected the pups’ brain development (Tang et al., 1984). 

Mental pathology rooted in germ cell exposure: a scientific heresy?

Therefore, we can see that in the early 1980s two papers suggested adverse heritable effects of GA, showing mental impairment in the progeny via mysterious “genetic aberrations” or “genetic alterations” of female or male germ cells.

Now, one might think these findings would have raised some concerns in the medical community — surely, if GA agents could damage our sperm and eggs’ genetic material in a way that caused learning deficits in the next generation, that is something doctors and patients would wish to know. But instead what followed was the opposite of scientific scrutiny — decades of absolute silence with absolutely no follow-up research that we could find.

Though it’s difficult to say why the germ cell exposure idea hit a wall, it seems possible that the observations reported by Turndorf’s lab fell victim to the weight of conventional dogma about inheritance. It was broadly accepted at that time that heritability of traits depended on genes from our parents, except in those rare cases where genes suffered a random mutation. The dogma left no room for other ideas about molecular sources of inheritance, such as the quasi-genetic forces we discuss here, forces that did not rise to the level of a full genetic mutation. The GA agents were not thought to be mutation-causing, so the idea that GA could induce a heritable brain pathology amounted to a sort of scientific heresy. The idea, it appears, became scientifically orphaned. Abandoned.

Looking back on my years in medical training and anesthesiology practice, I (LDF) should note that not once did the question of heritable effects of germ cell exposure to GA come up. Germ cell effects were not mentioned in medical school, residency, FDA advisories, research papers, conferences, or professional literature. It was as if germ cells were almost presumed to be immutable marbles, impervious to even the most toxic chemical influences like GA.

In a Florida lab, “epigenetic inheritance” links germ cell exposure to mental impairment

Now, fast forward from 1980s New York City to a few years ago in Gainesville, Florida. In the early 21st century, cracks in the edifice of genetic determinism began to appear, and these became known to Dr. Anatoly Martynyuk, Professor of Anesthesiology and Neuroscience at the University of Florida, who researches developmental neurobehavioral impacts of general anesthetic agents. The professor, while not familiar with the Turndorf studies, had read a series of animal studies demonstrating that acute stress and trauma could impact the molecular content of egg and sperm, resulting in altered brain and behaviors in the offspring, one of the new lines of research demonstrating mechanisms of non-genetic inheritance (see, eg, Bohacek and Mansuy, 2015). So he started thinking beyond the GA-exposed brain to consider the exposed germ cells as well.

Perhaps, he thought, GA could be meddling with molecules inside nascent eggs or sperm. 

The previous decade of research demonstrated that common GA agents such as halothane, enflurane, and sevoflurane could not only influence neuronal function, but also induce epigenetic and chromatin modifications, though this work was not done in germ cells in particular (Csoka et al., 2009; Pan et al., 2006; Rampil et al., 2006; Jia et al., 2016; Vutskits et al., 2018). Again, these changes include molecular alterations to the DNA three-dimensional structure and chemical tagging of DNA, perturbing the way genes are expressed. For example, even brief exposure to the GA agent isoflurane led to widespread changes in genetic control in a brain region called the amygdala six hours after exposure (Pan et al., 2006). 

So, hypothesizing that GA exposure to early germ cells could cause a direct “epigenetic inheritance” by changing how germline genes function, Martynyuk’s group undertook an experiment. They exposed both male and female neonate rat pups to sevoflurane, the most popular GA gas used in pediatrics, and then looked at brain, gene expression, and behavior in the next generation, taking care to assess sex-specific effects, since sperm and egg are epigenetically distinct. Remember learning about meiosis in high school? Egg and sperm travel very different developmental paths, and that includes the content of their epigenomes.

The lab used a sub-clinical dose of sevoflurane because a clinically relevant dose would have resulted in low oxygen levels and other abnormalities in the pups’ blood (use of GA generally requires use of a breathing apparatus to keep the patient alive, something the researchers could not do in this case). With limited funding they only looked at only two parts of the brain (hypothalamus and hippocampus) and the expression of only two genes. But it was a start, and as far as they knew, it was the first study to examine the heritable impacts of GA.

After assessing the effects on the directly exposed pups (which predictably suffered some impairments) the team looked at brain, gene expression and behavior outcomes in the following generation, which we’ll call “progeny,” borne of the pups’ GA-exposed germ cells. 

They found that the male, but not female, progeny showed signs of neurodevelopmental impairment. Progeny of exposed males, that is, of the exposed sperm, had abnormalities in the maze test, suggesting impaired cognition, abnormalities in prepulse inhibition of startle, suggesting decreased ability to filter out unnecessary information, and decreased expression of a gene in the hypothalamus. Where both parents were exposed, male progeny exhibited impaired spatial memory and decreased expression of the gene in both the hypothalamus and hippocampus. An analysis of epigenetic changes in sperm of exposed males and brains of progeny revealed gene expression shifts not present in control rats. In other words, it appeared that the male rat progeny, exposed only during the early germ cell stage, exhibited behavioral impairments connected to sevoflurane-induced epigenetic modification (Ju et al., 2018).

It was not a stop-the-presses sort of study, given the limited scope of investigation, the sub-clinical doses of the drug, and the subtleties and oddities of some of the findings. But it was nevertheless suggestive that GA seemed to induce a non-genetic effect in early-stage germ cells, causing some sex-specific brain and behavioral abnormality in the next generation. And this time, it seems, the lesson was not entirely lost on the medical community. 

A British Journal of Anaesthesia editorial accompanying Martynyuk’s paper, and also citing the first Turndorf study, touched on the possible public health implications of the new findings. The commentary, evocatively titled, “A poisoned chalice: the heritage of parental anaesthesia exposure,” noted that “we are faced with a real possibility that general anaesthetics are not innocuous agents that ‘only put children to sleep’ but rather formidable modulators of chromatin remodeling and function” perhaps modulating developmental neuroplasticity in the next generation (Vutskits et al., 2018).

The importance of “critical windows” in germ cell exposures

Now, you are probably thinking, and you would be correct, that this is all very interesting but GA exposure to germ cells can’t generally cause autism, because otherwise nearly all kids would have autism. After all, a great many parents have had general anesthesia at some point in their pre-conception lives, whether for a tonsillectomy, appendectomy, something dramatic like major heart repair, or perhaps birth under sedation for a C-section. And clearly, although autism has increased markedly in prevalence, it’s still limited to about 1-2% of the childhood population. Common sense suggests gametes must be largely protected from damage.

But we are not suggesting such widespread havoc at all. Instead we should think about what scientists call “critical windows,” and also dosages. You see, it’s not just the substance itself, but the timing and the dose that make the poison. You may remember, for example, the story of a sedative drug called Thalidomide which came into use in the late 1950s. That drug often caused horrific birth defects such as missing limbs — but only if consumed in a certain early weeks of embryonic development. After that phase, this acutely toxic drug had fairly benign effects.

“It’s not just the substance itself, but the timing and the dose that make the poison.”

A similar timing-matters phenomenon exists with germ cells. Now bear with us because here we must delve into more molecular biology. Early in their careers, during the fetal period and, for girls, also the infancy stage, human germline DNA undergoes a dynamic de-nuding and redecorating unlike any sequence of events in other cells.

The germ cells, in order to give rise to an entire new organism, need to shed old epigenetic rags and dress themselves with new epigenetic finery consistent with their sex, male (sperm) or female (egg). Broadly called germline reprogramming, this process sees the germ cells’ DNA become “demethylated,” “remethylated,” and “imprinted” in sex-specific ways. At the same time it appears that the chromatin and the protein spools that wrap DNA, called histones, also get remodeled. Together with other mechanisms, these are the marks (or absence thereof) that will fine-tune development. Our germ cells are “immortal” — descending from millions of years of organismal continuity — because of this elaborate molecular ritual that imbues them with new youth and totipotent superpowers.

You could imagine these molecular processes a bit like a game of musical chairs. The young denuded DNA extends like the line of empty chairs. The chemical tags that attach to and fold the DNA swarm like the kids running around looking for an open seat. DNA function will ultimately change depending on what chairs end up occupied by what kids, and how much those chairs get pushed around. 

Oversimplistic, absolutely, but it gives you a sense of the dynamism present in the early germ cell, which contrasts with later developmental stages in which germ cells tend to be somewhat sleepier. Once the kids find their seats, the music stops and they sort of hang out, for years. Male germ cells, however, feature some notable additional epigenetic and genetic vulnerabilities from puberty onward due to the vagaries of spermatogenesis. Picture the girls lounging in their seats, but the boys pushing more chairs around as they hit puberty. Therefore, for men in particular, pubertal or later exposures (for example, drugs or tobacco) could damage the molecular program in their germ cells.

“A potent, epigenetically active drug like GA, delivered in the right time, duration and dose, could interfere with how the genome gets folded and decorated. Some of those quasi-mutations can persist post-conception, into the offspring born years or decades later.”

Enough biology — we know this is difficult, thank you for bearing with us — and back to the bottom line. A potent, epigenetically active drug like GA, delivered in the right time, duration and dose, could interfere with how the germ cell genome gets folded and decorated. Some of those glitches can persist post-conception, into the offspring born years or decades later, exerting outsize, and rather unexpected, effects on gene expression. Thus, we can have a quasi-genetic impact on health and development.

Autism family stories raise red flags

Okay, so certain exposures like general anesthesia might tinker with our germ cells. But what does it mean for autism? A handful of animal studies finding neurodevelopmental impairment hardly amounts to a closed case. Well, regrettably there appear to be no published papers on heritable effects of GA in humans, which strikes us as a galactic, scream-worthy gap in the research, considering the magnitude of synthetic volatile GA use since the 1950s. So of course it’s impossible to draw any conclusions.

But perhaps it’s useful to begin where human research often starts, by simply listening to families and hearing their stories. Might their reports raise some red flags? While this is hardly science, we wanted to share a sampling of autism family stories that seem to do just that.

A mother reports her mother had an appendectomy while pregnant with her. She has two girls with idiopathic autism. A mother said her mother had surgery when pregnant with her, following an automobile accident. She has three boys with idiopathic autism. Two different fathers report having had a series of complicated surgeries after suffering teenage gunshot wounds. Both have sons with profound forms of idiopathic autism. Two different parents, one female, one male, had open heart surgery in early childhood to repair heart defects. Both have sons with idiopathic autism. A mother states she had two surgeries as a neonate, one to remove a benign tumor and another to repair a hernia. She has two sons with idiopathic autism. A father’s mother said she had surgery when pregnant with him, to correct a placental problem. The father has a son with idiopathic autism. A mother had early childhood surgeries to repair a cleft palate, She has a son with idiopathic autism. Now, these are mere anecdotes without control groups. But from evidence when available, as a makeshift control group where the autism parents’ siblings were not exposed to early surgery (and therefore GA) there were no other family cases of autism.

Still, as we said, this is at best hypothesis hunting and certainly not science. And who knows what if any genetic predisposition or other exposure questions may have lurked in the parents as well. But our point in sharing the family stories is not to convince you that parental germ cell exposures to GA can raise the risk of autism in progeny — as we said, there has so far been zero research in humans. Instead, we are suggesting these stories, reflecting strong patterns of heritability, combine with lab science and textbook knowledge on GA impacts to present an exquisitely important question for research: are some cases of “heritable” neurodevelopmental pathology not genetic at all, but rather quasi-genetic and induced by long-forgotten germ cell exposures? We can only find out if we first ask the question.

As a former anesthesiologist (LDF), let’s be clear. This is not about blame or antagonism toward necessary drugs or especially GA, which is by all accounts one of the great medical advances of the modern age. If you want to get a sense of the surgical horrors endured by humans before the advent of GA, we invite you to watch this documentary, Scream: The History of Anaesthetics. A great many readers of this article are alive today thanks to the miracle of modern GA, whose sedative and hypnotic effects enabled the practice of modern surgery. Our gratitude for GA should overflow, but at the same time we should be cognizant that these agents are powerful poisons that may invite unintended consequences.

So far we have used GA as an example toxicant, but when it comes to contemplating the reality of families’ biological histories, a great many other exposures should also concern us.

Drugs aplenty in the post-war womb

Synthetic drugs, including those used in pregnancy, boomed during the postwar decades. In addition, maternal smoking peaked in the 1960s. Some examples of common pregnancy drugs from the 1950s and 60s, pictured clockwise from top left: anti-nausea, anti-anxiety, synthetic steroid hormones [pictured here, an ad for the notoriously toxic drug DES], volatile anesthetic gases, tobacco, barbiturates, amphetamines/methamphetamines.

Why now? Why the steep increase in autism starting with births in the early 1980s? It’s a baffling mystery seemingly without any explanation. So a song springs to mind, “Don’t know much about history… don’t know much biology...” because it seems if we don’t know much about our biological histories, we may never piece this puzzle together.

There’s no nice way to put it: the American womb became something of a chemical soup in the decades after World War II. As writer Annie Murphy Paul observed, the post-war years saw a staggering increase in the use of synthetic pregnancy drugs. “The middle of the twentieth century was a golden age of pharmaceutical innovation, a time when serene sleep and steady nerves and a slim figure could be found inside the medicine cabinet,” she writes. “Pregnant women, too, were promised relief from all the complaints, small and large, of their condition: sleeplessness, morning sickness, miscarriage… those who gave birth in the postwar years, writes one chronicler of the period, ‘were among the most medicated women in history’” (Paul, 2010).

Pregnancies of the post-war era were often heavily medicated with chemical compounds that were entirely unprecedented in the human womb. Here, for example, a medical record from 1965 shows that a pregnant woman in Boston was prescribed synthetic steroid hormones, diuretics, anti-nausea drugs, analgesics, and sedatives, among other drugs such as insulin for Type 1 diabetes. While any quasi-genetic impact is of course unknown, it is worth noting that three of the woman’s grandchildren exhibit multiple idiopathic neurodevelopmental abnormalities.

Synthetic hormones, barbiturates, amphetamines, diuretics, analgesics, sedatives, anti-anxiety medicines, tobacco. All of these were rampantly used in pregnancy, typically under doctors’ orders. It was not uncommon for pregnant women of the 1950s and 60s and even the 70s to take upwards of a dozen prescription and over-the-counter drugs for common or serious complaints. The placenta was presumed to provide a barrier to harm, pregnancy drugs were seldom evaluated for safety or efficacy, and women at that time tended to trust without question the advice of their physicians.

[On a personal note, back in the 1960s co-author JE was exposed in utero to an intensive eight-month protocol of synthetic steroid hormone drugs, a history detailed in Bugs in the Program (Escher, 2018), while co-author LDF was exposed in utero to tobacco smoking.]

Meanwhile, of course neither regulators nor physicians considered potential impacts of all these drugs on the exposed fetus’ germ cells. It amounted to a vast uncontrolled chemical experiment, with wholly unknown generational implications. But today the tide is turning, and finally researchers are beginning to examine links between drugs, germline disruptions, and impairments in offspring, including impacts on brain and behavior. Beyond the previously discussed general anesthetic agents, here are some examples from the research literature:

Steroid hormones

Steroids are little molecules that help orchestrate development by changing gene expression. Synthetic, lab-made steroid hormone drugs, including gender-bendy fake sex steroids, came into widespread use in pregnancy in the 1950s and 60s. Many people will remember, for example, the toxic synthetic estrogen, diethylstilbestrol (DES) one of the greatest medical disasters in history. While this drug was taken by millions of pregnant women for the ostensible prevention of miscarriage, it was in fact ineffective and often carcinogenic (causing reproductive cancers) and teratogenic (causing birth defects such as penile and uterine malformations). In repeated mammal and human studies, DES has been linked with grandchild pathologies such as cancer and reproductive dysfunction, suggesting germ cells were tainted by the pseudo-hormone’s disruption of normal cell signaling (see, eg, Titus et al., 2019). And notably, last year significantly elevated odds for attention deficit hyperactivity disorder (ADHD) were found in grandchildren of women who took DES during pregnancy (Kioumourtzoglou et al., 2018). 

Other synthetic steroid hormones have been seen to cause brain/behavior impacts in the germline progeny in animal models. Gestational treatment with the synthetic glucocorticoid betamethasone resulted in modified brain function and behavior in guinea pigs (Moisiadis et al., 2017; Iqbal, et al., 2012). Exogenous thyroid hormone influenced brain gene expression programs and behaviors in later generations by altering germ line epigenetic information in a mouse model (Martinez et al., 2018). 

It is also worth noting that in animal models, germ cell exposures to hormone-disrupting environmental chemicals have also been shown to alter brain and behavior of the offspring borne of exposed cells. For example, exposure of rats to the common fungicide vinclozolin and pollutants called PCBs at the germ cell stage led to differences in the physiological and socio-sexual phenotype in offspring, especially in males (Krishnan et al., 2018). Gestational exposure to the same compounds in rats resulted in inheritance of epigenetic errors in brain and sperm (Gillette et al., 2018). Exposure to BPA, a common plasticizer, can cause generational effects on gene expression and DNA methylation of imprinted genes in the mouse brain (Drobná et al., 2018; Wolstenholme et al., 2012).

Tobacco, tobacco components

Although it is hard to imagine now, maternal smoking was once very common. In fact it was not unusual for obstetricians of the post-war decades to prescribe smoking (and/or amphetamines) to pregnant patients as a means for weight control. This was an era in which gestating women were often instructed to not gain more than 20 pounds, and weight control measures were sometimes draconian. Unfortunately, tobacco smoke, with its hundreds of toxic chemical components, is now known to induce a wide variety of molecular aberrations in exposed tissues. This extends to germ cells.

In the first human study of its kind, grandmaternal smoking was linked to autism and autism trait risk in grandchildren through the exposed female line (Golding et al., 2017). Animal models suggest the biological plausibility of this finding. Grandpups of gestating mice exposed to nicotine exhibit hyperactivity and risk-taking behaviors (Zhu et al., 2015; Buck et al., 2019), apparently owing to alterations in gene expression in the offsprings’ brains (Buck et al., 2019).

In adult male mice, nicotine exposure also produces behavioral impairment in progeny (hyperactivity, attention deficit, and cognitive inflexibility) (McCarthy et al., 2018). Germ cell exposure to the toxic tobacco smoke component benzo[a]pyrene increases levels of germline and somatic mutation (called mosaicism) in offspring, particularly in the brain (Meier et al., 2017). The renown genetic toxicologist David DeMarini of the U.S. EPA has argued that tobacco should be considered a germ cell mutagen (DeMarini, 2012). These and other early studies are scratching the surface of the mostly unexplored realm of heritable effects of smoking, an important subject that for the first time will be the focus of a scientific workshop in Washington, DC in September 2019 (emgs-us.org).

Opiates

We are in the midst of an opioid epidemic, and, worryingly, evidence is emerging that opiates could have neurobehavioral impacts on the next generation via exposed germline (Vassoler et al., 2018; Sabzevari et al., 2018; reviewed generally in Gilardi et al., 2018).

While we have focused on brain and behavior in this discussion, other studies have demonstrated how drug, smoking or chemical exposures to germ cells can increase risks for other pathologies as well, including cancer, metabolic dysfunction and obesity, asthma and allergies, even differences in sexual behavior. Research has reported some perplexing links between autism and these conditions, and perhaps the quasi-genetic phenomenon will help explain some of them.

[Another note to biology buffs: See here for a compilation of more than 100 studies demonstrating non-genetic inheritance in humans and mammals.]

Intriguing consistencies with patterns seen in autism

It’s not every day that a hypothesis of autism comes along that can help explain many of the baffling patterns seen in the research literature. But we think this quasi-genetic hypothesis packs an unusual punch when it comes to potential explanatory power. Here are some examples:

• Temporal associations. The start of the autism increase, observed to have begun with births in the 1980s, comes roughly a generation after early germ cell exposures to these novel synthetic pregnancy drugs and the peak of maternal smoking (1950s and 60s).

• The 4:1 male:female sex ratio. The hypothesis is consistent with the sex-specific intergenerational responses to exposures detected in human and animal studies. Several studies in hormonal disruption of germ cells, for example, have found male offspring more likely suffer adverse effects.

• Autism heterogeneity and the “broader autism phenotype.” Toxicant exposures to male or female germ cells over different times, in different doses, in different combinations, against a backdrop of varying genomic susceptibilities, would likely not cause uniform effects. This roulette-wheel mix could help explain the heterogeneity of the autisms and “broader autism phenotype” seen among other family members. Also the personalities and cognitive traits of parents themselves could have been influenced by their direct in utero exposures, as was the documented case with co-author JE who was a subject in this landmark study on developmental impacts of synthetic steroid hormone pregnancy drugs (Reinisch and Karow, 1977).

• Regional, socioeconomic, and ethnic disparities. Higher rates of autism in some regions, ethnicities and socioeconomic strata may coincide with higher rates of drug exposures of the parents, for example, pregnancy smoking in the grandmother generation.

• Missing heritability of autism. As discussed above, quasi-genetic effects could help explain the contrast between the strong heritability of autism and the surprisingly shallow findings from traditional DNA-sequence-focused genetics.

• Arising in early brain development. It has been frequently observed that autism arises from brain mis-wiring during early development in the womb. What drives this mis-wiring? Increasingly it looks like chromatin and epigenomic factors may contribute, suggesting that “epigenetic dysfunction is a fundamental contributor to brain development and disease pathogenesis of neurodevelopmental disorders, including ASD” (Tremblay and Jiang, 2019).
  

Quasi-genetics as a new priority for autism research

Though we feel this hypothesis is strong, we do not remotely suggest that all autisms are quasi-genetic, or that other hypotheses are not worth exploring. Of course many are. But if we ever want to solve the mystery of autism’s heritability, research must embrace a greater degree of biological and historical authenticity. Today, we see too many researchers sitting in offices thinking in the abstract about even the weakest of genetic associations, while remaining unconcerned with any other information transmitted by germ cells, and totally disconnected from actual autism families and their complicated exposure histories. We continue to pour hundreds of millions of taxpayer dollars looking under the lamppost of gene sequencing, although it’s clear we’re in the land of diminishing returns chasing ultra-ultra rare variants with precious little relevance for families, prevention or public health. Meanwhile we spend pretty much nothing investigating heritable effects of exposures.

These questions could be researched in various ways. For example, rodent models can provide a rough idea of impacts of various drugs, such as those discussed in this article, on the next generation’s gene expression, brain function, and behavior. In humans, retrospective studies in populations with documented drug and smoking exposures could be conducted, even though of course researchers would need to be careful of “confounds,” or other factors that could be intervening to change outcomes. We suggest that the question of quasi-genetic inheritance is of such relevance and importance that our National Institutes of Health should consider funding at least 50 studies on this subject in the next three years. We dropped the ball in the 1980s when this idea first percolated. Let’s make up for all that lost time.

It is a heartbreaking possibility that errors of brain development could be an unforeseen legacy of certain benign-seeming actions that occurred very long ago. But given the potentially significant public health implications, and the emerging science demonstrating biological plausibility, it’s time to reconsider the history of our germ cells, and what those histories mean for our children.

La Donna Ford, MD is a former anesthesiologist. She is the mother of a son with idiopathic autism and lives in the San Francisco Bay Area.

Jill Escher is a research philanthropist (GermlineExposures.org), president of the National Council on Severe Autism, president of Autism Society San Francisco Bay Area, and a councilor-elect of the Environmental Mutagenesis and Genomics Society, where she also serves as chair of the Germ Cell and Heritable Effects special interest group. A former lawyer, she is the mother of two children with idiopathic autism and lives in the San Francisco Bay Area. 

Correspondence may be directed to jill.escher@gmail.com.

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