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A 2014 Medicaid guidance, now withdrawn, had the effect of substantially restricting program and residential choices for autistic adults precisely at a time of surging need for new options.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

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:

  •  “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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Stock photo



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.


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Stock photo



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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Stock photo



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

Martha Moyer Pic.png

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.]

“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.

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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 )

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.

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.

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.

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.

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).

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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).

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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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Medical Cannabis: One Mother’s Journey with Her Severely Autistic Son

Out of options and out of time, a conservative but desperate mother turns to medical cannabis to help her son. The experience turns her into a national advocate.

Nate on his third day of cannabis, in June 2015. A genuine smile, in Joshua Tree, California.

Nate on his third day of cannabis, in June 2015. A genuine smile, in Joshua Tree, California.


By Jenni Mai

“Are you looking for indica?”

That was one of the first questions thrown at me when I made my maiden voyage into a California medical cannabis dispensary in 2015. I remember looking at the girl who was waiting on us and thinking, “I don’t know who this ‘Indica’ is, but if she can help me figure all of this out, please send her my way!” 

I was desperate, scared, completely ignorant, and admittedly… I even felt a little dirty. 

I am a married mother of three! From a pretty conservative family from the Midwest! What will people think of me? What am I doing in here… with my son? 

 After taking a deep breath, I remembered that my son needed me to figure this out. We were out of options and out of time.  

“He’s just too aggressive”

Three months before this scene we were living in Missouri, where my family, Wisconsin natives, moved due to a career advancement opportunity for my husband. We thought this relocation 450 miles down I-55 would be great for our family, but it turned into a nightmare.

All three of my sons are on the autism spectrum. Nate, my guy in the middle, is by far the most severely impacted of the three. He’s nonverbal and had a long history of extreme aggression and self-injurious behaviors. We made countless (failed) attempts to get any sort of short-term inpatient treatment to keep him and our family safe. We soon found out the only thing available to him was more and more pharmaceuticals and less actual mental health or social service help.  

His high school decided he was not a candidate for the transition program that should have been available to him until he turned 22. Instead, they handed me his diploma when he was 18 and sent us on our way to nowhere. A day program that reluctantly took him in ended up sending him home early on an almost daily basis because they also apparently could not handle his level of need. 

Just a few months after starting, they wrote him off for good. He’s just too aggressive. Then things got worse. 

During this constant battle of trying to help my son, I came across a news clip about a family on the west coast that started treating their son’s extreme behaviors with cannabis. I saw that young boy’s badly bruised and bloodied face peering out from under the bright red protective padding of his wrestling headgear and I watched his parents speak about his self-inflicted harm.  They shared how an “oil” of some sort was greatly reducing these behaviors. I had never felt more perplexed in my life as I watched the story over and over.

Holy cow - they’re giving that little kid WEED?!  What kind of par-… wait… he stopped punching himself? He’s sitting calmly and smiling? Come on now, Is this really a thing? Seriously? 

Right around this time, we were looking to relocate again. Missouri clearly turned out to be a bad situation for us and we needed to go someplace that offered Nate more than just a lifetime of monster doses of antipsychotics and benzodiazepines. We knew that going home to Wisconsin wasn’t going to make anything better. California came up as an option and I saw that they had medical cannabis. 

This is it. We have to try it. If this doesn’t work, we will have to find alternative placement as soon as possible. He’s not safe. We’re not safe. We cannot keep doing this the way we are. It’s just not working. At that point, we have nothing left to lose…except for my son.

The move to California

Nate on our way to California in March 2015.

Nate on our way to California in March 2015.


After we got our California residency, schools, and services started, I quickly turned my focus back to what I felt was our Hail Mary. I searched the internet for cannabis doctors and found one nearby. While he was such a nice guy (and I consider him a dear friend to this day and instrumental in saving my son), he was barred from giving me anything beyond the written medical cannabis recommendation due to the federal law that threatens physicians’ medical licenses if they “prescribe” it.  

Extremely confused, Nate and I walked out of his office and started heading to a dispensary that I had seen near my home, complete with a flickering neon Green Cross and blacked-out windows that were flanked by four burly security guards. My head was spinning and to say I felt overwhelmed is an understatement. Did I mention that I felt a little dirty walking in there?   

But my dear indica. You had me at hello. 

At the dispensary, I was given a 10mg THC edible and a vape pen. I was a bit hesitant about encouraging my son to inhale cannabis from a cartridge and battery that resembled an e-cigarette, but desperate times called for me to model it for him and hope he would follow my lead. Because of the shape and size of the vaporizer, the first thing I thought of was to compare it to drinking through a straw. I put a straw in a glass and said “drink!” while I took a sip. I then gave him the glass and straw and said “drink!” again. He complied. Next, I pulled out the vaporizer, held it up in front of him, said the word “drink!” and I inhaled from it. Then I held the vaporizer up to his mouth, once again said “drink!” and he immediately copied what I did. Within 10 minutes of giving my son his first dose, I could see a calmness I hadn’t seen in a long time.

On day three, we took a drive out to Joshua Tree National Park. I gave him a dose before we left the house and he spotted me taking pictures of the beautiful landscape. My son, who rarely smiled for a photo, plunked down and gave me the most beautiful grin I had ever seen without me even prompting any of it. It wasn’t the typical distant, vacant stare I normally got from him; it was a real smile. Genuine happiness. A “presence” I may have never seen in his almost 20 years. He cannot tell me how he feels, but I can see it. It is crystal clear that he is in a much better place.      

Seven months after starting cannabis, Nate no longer needed any of his psychotropic pharmaceuticals (never attempt to reduce or remove medications on your own – you must be under the guidance of a medical professional and similar results are not guaranteed). He went from 18 pills a day to zero. ZERO! He’s safe. We’re safe. We were all living happily together under the same roof and enjoying life. He even started going to a day program again, where he enjoys spending time with his peers.

We have adjusted Nate’s cannabis intake up and down over the years. We have found many variables that have determined how much he would likely need. While Nate was weaning from all of the pharmaceuticals under a doctor’s guidance, he needed his cannabis intake increased over time to not only compensate for the medications, but to help mitigate withdrawal symptoms as well. His doses of THC were quite large for a period of time but have since greatly decreased.

Onward to advocacy

At a local community autism group early in our cannabis journey I met my future business partner and fellow autism mom, Rhonda Moeller. She’s got a young daughter on the spectrum and had also begun to look at cannabis to treat some of Maliyah’s symptoms before heading down the pharmaceutical path. We decided to form a support group on the same social media platform where we met.  

Rhonda’s background as a biochemist became an invaluable asset to not only me, but to the handful of other families who voiced their cannabis curiosity. The handful grew to a few hundred, then a few thousand, and today we have nearly 14,000 members in our online community. As we grew, we read their pleas for help and we began looking for ways to offer as much educational assistance as we could.   

In early 2018, we were granted a 501(c)(3) tax exemption and officially became the nonprofit organization WPA4A, Inc., more commonly known as Whole Plant Access for Autism. While we are not doctors, we are able to help educate families about medical cannabis. We collect information from every study we can find and explain the researchers’ findings to our members. We also collect a variety of anecdotal data from our own members and Rhonda creates beautiful graphs to help everyone see the different ways our families feel that it helps their children. 

We also work with another nonprofit organization, MAMMA (Mothers Advocating Medical Marijuana for Autism), and connect our families to them when they want to help get autism added to the list of qualifying medical conditions in their states. Currently eleven states recognize autism as a qualifying condition, another handful where adding autism is currently being discussed, a few others with broadly-encompassing “debilitating” or “neurological” conditions, and finally, many that list common co-morbid conditions that may qualify many of the children of our members. 

Based on the surveys we take in our support group, we have seen parents report that positive effects greatly outweigh negative responses. The following WPA4A graph shows our families’ self-reported results of three of the major cannabinoids: THC, CBD, and CBG.    

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WPA4A works to educate our families on everything from the most basic cannabis information (I’m looking at you again, indica) to more complex scientific information and studies, which helps our families become as informed as possible so they can navigate the cannabis maze as safely and confidently as they can, while they hopefully can shorten any trial-and-error period. While there is no magic bullet and no one-size-fits-all, there are countless cannabis options to try if one is so inclined. From better sleep to less aggression and lower pharmaceutical doses for some of our families, you can read some family testimonials here.   

Based on reports to us, families seem to have the most success with tinctures, cannabis-infused oils, vaping, and plant matter capsules. Pre-made gummies and other edibles tend to be hit-or-miss because they generally do not include strain information, which could make a significant difference in success or failure. Topical creams and lotions do not appear to be very effective for symptoms like behavioral issues but could work well for skin conditions or localized pain.  

Always consult a doctor before trying any new medical treatment. With cannabis becoming increasingly legalized and more widely accepted by the medical community, doctors are beginning to see more families asking about it as an option. While less pharmaceutical usage may be appealing to some, you must work with your doctor to see if that would be an option for your particular situation. Never attempt to start, change, or stop a medication without discussing it with a medical professional who is familiar with the patient. WPA4A does not provide medical guidance; we simply provide cannabis education, so our members have information to discuss with their doctors.  

Depending on the laws of your state, you may need to seek specific cannabis doctors in order to become legal patients and/or cannabis caregivers for your loved ones. We can be reached at info@wpa4a.org if you would like help locating a cannabis doctor in your area. Even if you live in a “legal” state with recreational/adult use access, anyone under the age of 21 must be a part of the state’s medical cannabis program in order to use it legally. If you do not have a medical cannabis program in your state or if you are unsure of your laws, please reach out to our friends at MAMMA in order to find out more about that topic.  

There is hope.

Jenni Mai is the President and co-founder of WPA4A, Inc. She lives in Southern California with her family and is a graduate student at Louisiana State University, Shreveport, pursuing her Master of Science in Nonprofit Administration. She can be reached at jennimai@wpa4a.org

Dr. Orrin Devinsky

Dr. Orrin Devinsky

Editor’s note: You can learn more about the question of cannabis for autism in this video featuring Dr. Orrin Devinsky at the 2018 Autism Science Foundation Day of Learning in NYC.

Disclaimer: The information provided is intended for your general knowledge only and is not a substitute for professional medical advice or treatment for specific medical conditions. You should not use this information to diagnose or treat a health problem or disease without consulting with a qualified healthcare provider. Please consult your healthcare provider with any questions or concerns you may have regarding your condition. NCSA has not yet taken any position with regard to medical cannabis.

Autism: Miswiring and Misfiring in the Cerebral Cortex

Autism is not a benign difference in brain function. Here, a neuroscientist explains a type of pathology often seen in the brains of autistic individuals — abnormal micro-structural development of the cerebral cortex — and an implication for potential intervention.

Human cortical development between 26 and 39 weeks of gestational age. (Image: Wikipedia)

Human cortical development between 26 and 39 weeks of gestational age. (Image: Wikipedia)


By Manuel Casanova, MD

Abnormal behaviors have roots in abnormal neurobiology, and autism is no exception. Notably, research on brains of individuals with autism indicates that micro-structures in the outer region of the brain, called the cerebral cortex, are malformed during early development. 

The cerebral cortex is the part of the brain that enables us to process sensory information, engage in complex thought and abstract reasoning, and produce and understand language. It accounts for our volitional actions including those that allow us to adapt to our immediate environment. These functions align with many of the deficits seen in patients with autism.

In autism, perhaps not surprisingly, we have often seen that cortical development goes awry. As a fetus develops, brain cells migrate from a germinal area to their proper locations, but in autism, cells destined to move into the cerebral cortex undertake an abnormal migration. Sometimes instead of completing their migration, these cells get stuck in the wrong location (Casanova, 2014). The end result is failure of connections — cells in the cerebral cortex are not able to coordinate their actions with other cells in their surroundings.  

“The end result is failure of connections — cells in the cerebral cortex are not able
to coordinate their actions with other cells in their surroundings.”

Image: The cerebral cortex is a highly organized brain structure. In early development, brain cells, labeled (a), surround the core cavities of the brain before they migrate to the cortex. They make their way through the white matter of the brain in order to reach the cortical plate (b), or future cerebral cortex. In autism, this process is often disrupted. (Image courtesy of Dr. Manuel Casanova)

Image: The cerebral cortex is a highly organized brain structure. In early development, brain cells, labeled (a), surround the core cavities of the brain before they migrate to the cortex. They make their way through the white matter of the brain in order to reach the cortical plate (b), or future cerebral cortex. In autism, this process is often disrupted. (Image courtesy of Dr. Manuel Casanova)

These findings are quite evident in microscopic studies of the post-mortem brain. Wegiel and associates (2010) reported evidence of pathological markers in 92% of the cases they examined. The changes in terms of severity and location vary from patient to patient. The findings of pathology, however, are frequent enough for researchers to propose the use of MRI techniques that detect atypical cortical development as a way to subtype autism spectrum disorder (ASD) patients (Andrews, et al., 2017).

Abnormal mini-columns in autism

The brain is a “modular” organ. A module is an independent unit that along with other similar ones construct more complex structures (Lego blocks, for example, may be regarded as examples of modular structures). This organizational scheme allows for the integration of different tasks while simultaneously allowing the independence of its constituent units. 

In the cerebral cortex, connectivity within modules far outpaces the connectivity between modules. Cells that work together are as close to each other as possible. This pattern of connectivity establishes a microcircuit which is repeated millions of times throughout the cerebral cortex (Casanova et al., 2018).  

Sometimes migratory cells get stuck in locations where they should not be present. In this photograph they are present as nodules abutting the central cavities (ventricles) of the brain. These cellular agglomerations are usually foci of seizures. (Image courtesy of Dr. Manuel Casanova)

Sometimes migratory cells get stuck in locations where they should not be present. In this photograph they are present as nodules abutting the central cavities (ventricles) of the brain. These cellular agglomerations are usually foci of seizures. (Image courtesy of Dr. Manuel Casanova)

The smallest module capable of processing information within the cerebral cortex is called a “minicolumn.” It was given this name because the cells in these modules have a radial or columnar arrangement. You can think of the minicolumns like microprocessors in a computer. Minicolumns are the central processing unit that contain within themselves all the necessary functions to process information and execute a response.

Recent research suggests that the genesis of higher executive functions — mental skills that control other brain processes — stems from our minicolumns. Impairment of these functions contributes to poor cognitive and social function that ultimately impedes adaptation to novel, complex, or ambiguous situations.

“Impairment of these functions contributes to poor cognitive and social function that ultimately impedes adaptation to novel, complex, or ambiguous situations.”

In autism, the minicolumns are abnormal. They seem to be closer together than in controls, suggesting their overall increase in numbers. This, by itself, is not bad. A minicolumnar variation that provides for discrimination and/or focused attention may help explain the savant abilities observed in some autistic people and the intellectually gifted (Casanova et al., 2007).  

However, in autism, the closeness of minicolumns seems propelled by a loss of tissue surrounding these modules. This peripheral space has been described as a shower curtain of inhibition that helps keep information inside the minicolumns. A faulty shower curtain, as in autistic individuals, allows for information to seep into adjacent minicolumns procreating a runaway excitatory cascade. 

The vertical configuration acquired by migrating neurons within the cerebral cortex provide a virtual ecosystem that establishes the excitatory/inhibitory bias in the brain. (Image courtesy of Dr. Manuel Casanova)

The vertical configuration acquired by migrating neurons within the cerebral cortex provide a virtual ecosystem that establishes the excitatory/inhibitory bias in the brain. (Image courtesy of Dr. Manuel Casanova)


Implications for intervention?

One might ask, if by knowing some of the anatomical and functional abnormalities in autism, can those findings suggest a therapeutic intervention focusing on core pathological aspects of ASD? One proposed therapeutic intervention in that regard is based on transcranial magnetic stimulation (TMS).

TMS works on the principle of induction of electricity. A strong magnetic field induces current through anatomical elements in the cerebral cortex that act as conductor. Due to the geometrical orientation of anatomical elements within the periphery of the minicolumns, inhibitory elements are stimulated when using low frequency stimulation.  This intervention allows us to rebuild the “shower curtain” surrounding the minicolumns.  

Thus far several hundred ASD patients have been treated with TMS with positive results, primarily in terms of improving executive functions and reducing stimulus-bound behaviors (Editor’s note: stimulus-bound behaviors are associated with perseveration on objects, a trait often seen in autism). That said, these studies have been limited to higher functioning individuals.


Despite the many limitations of post-mortem brain studies, actually looking at the microstructures of the brain offers the best opportunity for discovering the etiology of autism and proposing effective treatment. It is an exciting field where trained individuals can visualize the mechanics of life events, from neurodevelopment to old age, in a single microscopic slide. Each slide builds a story and the art of neuropathology resides in telling that story.

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Dr. Manuel Casanova is a researcher with extensive experience in neurology, neuropathology, and psychiatry. He is currently the SmartState Chair in Childhood Neurotherapeutics and Professor of Biomedical Sciences at the University of South Carolina/Greenville Health Systems.

He is the author of several books about autism, including the recent “Defining Autism: A Guide to Brain, Biology, and Behavior,” with Emily L. Casanova, PhD (Jessica Kingsley Publishers, 2019). Dr. Casanova also writes a popular blog corticalchauvinism.com that offers information about autism.

Editor’s note: It Takes Brains to Solve Autism

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Because post-mortem brain tissue is needed to study brain structure and development in autism, you might consider registering with Autism BrainNet. This is a research program where families can later make the heroic decision to donate brain tissue in the event of death of an autistic loved one.


Andrews DS, Avino TA, Gudbrandsen M, et al. In vivo evidence of reduced integrity of the gray-white matter boundary in autism spectrum disorder. Cerebral Cortex 27(2):877-887, 2017.

Casanova MF, Switala AE, Trippe J, Fitzgerald M. Comparative minicolumnar morphometry of three distinguished scientists. Autism 11(6):557-69, 2007.

Casanova MF. The neuropathology of autism. In Fred Volkmar, Kevin Pelphrey, Rhea Paul, Sally Rogers (eds). Handbook of Autism and Pervasive Developmental Disorders 4th edition, ch. 21. Pp. 497-531, 2014.

Casanova MF, Sokhadze E, Opris I, Wang Y, Li X. Autism spectrum disorders: linking neuropathological findings to treatment with transcranial magnetic stimulation. Acta Paediatrica 104(4):346-55, 2015.

Casanova MF, Casanova EL. The modular organization of the cerebral cortex: evolutionary significance and possible links to neurodevelopmental conditions. Journal of Comparative Neurology doi: 10.1002/cne.24554. [Epub ahead of print] Review. 

Wegiel J, Kuchna I, Nowicki K, et al. The neuropathology of autism: defects of neurogenesis and neuronal migration, and dysplastic changes. Acta Neuropathol 11:755-770, 2010

Family Separation, Autism Style

What happens when it’s no longer safe for an autism family to stay together?

Moving into their new home, Milton Hershey School.

Moving into their new home, Milton Hershey School.



“Mom, what is this place? Can I live here?”

My ten-year-old daughter and I were driving through the Milton Hershey School on Route 322. I looked out the window and knew she was right. She needed a way out. With these honest and painful words, my daughter helped our autism family find a better way.  

This is the story about why my husband and I decided to place our three typical children in a boarding school and keep our severely autistic, nonverbal son at home. 

My purpose in sharing is not to seek pity, but to expose the heartbreakingly difficult decisions we autism families often must make. All autism families have a tolerance threshold. We all need to respect this threshold and support each other. There are no clear answers when it comes to dealing with aggressive autism. We do our best, make difficult decisions, and keep going.    

“There are no clear answers when it comes to dealing with aggressive autism.
We do our best, make difficult decisions, and keep going.”

My husband and I have four children ages 6, 8, 10, and 12, and we live near Hershey, Pennsylvania. Our oldest, S, has severe, nonverbal autism and an intellectual disability. S is so much more than his diagnosis, and I've made this clear to him and to others. He loves riding rollercoasters, blowing out birthday candles, watching geese fly in formation, and the list goes on. His siblings are typical children who enjoy playing sports, going to parks, and spending time with friends.    

Ninety-seven percent of the time, S doesn’t have aggressive behaviors. I know that my family is fortunate because we are raising a child with autism who is happy and content most of the time. But S is driven by impulses that are usually unknowable and irrational, therefore he needs 1:1 care 100% of the time.     

You might ask if a family can be in crisis if the child’s behavior is violent only a percentage of the time. The answer is absolutely, yes. S’s siblings have had to learn how to move quickly, scream loudly, and get help. In a split second, S’s behaviors can change. He can go from sitting on the couch playing with a musical toy to chasing you down in attack mode. Noise, denied access, physical discomfort, changes in the environment, or other triggers can cause a crisis. I am ashamed to say that my children lived fearing for their safety in their own home. They screamed screeches no child should ever be in the position to scream. They endured hair pulls, scratches, hits, as well as having objects thrown at them. My children flinched and took cover when their brother moved too quickly or made a sudden, loud vocalization. They ran for cover under the kitchen table, hid in a bedroom, or darted out of the house.  

We did our best

We always believed that we could help S learn how to control his behaviors. He has made tremendous progress over the years and has been having much fewer aggressive outbursts. His self-injurious behaviors and aggressive behaviors towards others began when he was a toddler. These are deeply ingrained, habitual behaviors. We sought early intervention help when S was two years old, and two years later, we enrolled him at a private school for children with moderate to severe autism. He received a laundry list of therapies and home and community support. He learned how to communicate using picture cards, and then, he moved on to using an app on his iPad. I flooded my home with hours of therapy and fully believed that, with professional help, I could help my child.  

Even with a high level of skilled support, in January 2014, S’s aggressive behaviors toward his brother and sisters, as well as himself, were so extreme and frequent that our family decided we needed him in a hospitalization program. We went through the long process of waiting in a local ER for a bed to open somewhere in the state. Once we finally had our son placed, my husband and I immediately realized the plan wasn’t working. The staff would call us in the middle of the night asking how to calm him down. I would hear unfathomable screams and shrieks coming from S as he was causing self-injury. I could hear the pain, terror, and confusion in his cries. The staff didn't know how to manage his behaviors, I couldn't bring him home to hurt his siblings, and I couldn't live with myself as a mother knowing my child was suffering. S didn't understand why he was separated from his family. He was scared and far from home. We had very limited visitation hours, and the whole experience was horrible.  

So, my husband and I decided to bring him home, determined to make life work. During this time, I had a vivid dream I was drowning. This is exactly how I felt during this dark season. My family needed help, and I was going under. We tried to keep the kids safe, but S would still get to them. 

“I had a vivid dream I was drowning. This is exactly how I felt during this dark season.
My family needed help, and I was going under.”

We lived like this for four more years. Four more years. We had over 35 hours a week of professional help in our home, and we still couldn’t keep the kids safe. The guilt was overwhelming. I couldn’t get it right. How could I, an educator, who was able to connect with kids, not be able to help my own children? The screams of his younger siblings were branded in my mind. So we considered our options, wondering which one would be the least painful.

Desperately seeking a solution

A residential treatment facility would not have worked. S’s brief hospitalization was a disaster, S wouldn’t understand the new situation, it was distant from our home, and chances were insurance would deny or discontinue services. There was no stability.  

What if we relinquished our legal rights to S and gave him up as a ward of the state? I am ashamed to say we even discussed this option, but when you are desperate and your options are so limited, you comb every square inch. S would have guaranteed funding to have his basic care needs met. Insurance wouldn’t be able to deny residential care funding. BUT how could we bring ourselves to legally give up custody? We love S and this was never going to be a real option. We just had to talk about it and take it off the table.

We turned our thoughts to having our family separate. A family similar to ours was profiled on Australian 60 Minutes last year. The father stayed with the son, Max, and the mother moved with the siblings into a separate home. We felt this type of arrangement, where my husband lived with S and I stayed with the other kids, could give S’s brother and sisters the safety and stability they needed. The two roadblocks were financial feasibility and the fact of marital separation. We could overcome neither.  

So back to my drive with my daughter. The idea of enrolling our children at a boarding school was both heartbreaking and life-giving. The children needed and deserved to live in a safe environment. Milton Hershey School is a tuition-free boarding school that offers many academic, social, and athletic opportunities to its students. Houseparents and 8 to 12 students live in each of the 160+ homes within the campus neighborhoods. We toured the beautiful child-centered campus, spoke with staff, and witnessed how happy, loved, and well-cared for the students are. Our children needed a refuge from the storm, a place close to home, where we could pour out our love, and they wouldn’t feel abandoned. We prayed for them to be accepted — a hope didn’t come with joy, but with a sadness so tangible it made me feel nauseous for weeks.   

The decision

Sadness, anger, and hope rained down on us as we soaked in the news: they were accepted and we were enrolling them. My youngest responded with, “Six-year-olds aren’t supposed to live away from their mommies.”  My son, with tears in his eyes, blurted, “It’s okay to send me away instead of S, S wouldn’t understand.”  

Van packed up on enrollment day.

Van packed up on enrollment day.

How do you live without those daily hugs and kisses? How does a six-year-old adjust to having someone else reading her a bedtime story and taking care of her when she falls and scrapes her knee? How do you get used to driving by soccer fields where you used to watch practices and games? Separation was painful, but just like Max’s family, we were sticking with the plan. It was the only option.

Surprisingly, in some ways we are now more connected with our typical children because they aren’t living with the threat of violence 24/7. Survival mode is no longer ruling their lives. I don’t have to always be prepared to “save the day” and jump to their rescue. 

S's siblings are transitioning well to life on campus. As his brother stated last week, "It is starting to feel more like home, and I like it." S receives therapy services during the week, and he is making progress. We can challenge and push him a bit more because we don’t have to worry about the other children’s safety. There are fewer triggers in his home environment now, so S is calmer and is having less frequent outbursts. For the first time, I feel my family is finally living life.

Autism families can face incredible hardship. There must be a balance between the daily reality, and what you can change. We had to act, and like other families, had to find the least awful choice.

EF is a mother, wife, and educator living in Pennsylvania. She is passionate about advocating for practical, life-changing help for children and families.