Can pregnancy drugs disturb molecular reprogramming of the fetal germline ?

Bugs in the program: can pregnancy drugs and smoking disturb molecular reprogramming of the fetal germline, increasing heritable risk for autism and neurodevelopmental disorders?

2018 Study Abstract

In a seeming paradox, the prevalence of autism spectrum disorder (ASD) has surged, while at the same time research has pointed to the strong heritability of this neurodevelopmental pathology. Here an autism research philanthropist suggests a biological phenomenon of exogenously induced ‘gamete disruption’ that could reconcile these seemingly contradictory observations. Mining information from her own family history and that of her fellow autism parents, while also engaging with the scientific community, she proposes that a subset of the autisms may be rooted in a variety of molecular glitches in parental gametes induced by certain acute exposures during the parents’ own fetal or neonatal development. These exposures include but are not limited to synthetic hormone drugs, tobacco, and general anesthesia. Consistent with this hypothesis, animal models have demonstrated adverse neurobehavioral outcomes in grandoffspring of gestating dams exposed to hormone-disrupting compounds, tobacco components, and general anesthesia. A recent epidemiological study showed a link between grandmaternal smoking and risk for ASD in grandoffspring through the maternal line. Given the urgency of the autism crisis, combined with the biological plausibility of this mostly unexplored paradigm, the writer contends that questions of nongenetic inheritance should be a priority in autism research.

Read the full study (free access) Bugs in the program: can pregnancy drugs and smoking disturb molecular reprogramming of the fetal germline, increasing heritable risk for autism and neurodevelopmental disorders? on Oxford University Press, Environmental Epigenetics, Volume 4, Issue 2, 26 April 2018.

What Does the Future Hold for Autism Families?

Slides from the Autism in the Family Conference, February 2017

Presentation from the Autism in the Family Conference.

In Summary
  • Panic we’re not faking
  • Kool-aid—no more partaking
  • Policy we’ll be shaking
  • “i”nstitutions we creating
  • Spectrum needs some breaking
  • Smarter science is in the making

Time Bomb: a Journey into Old Exposures, Gametic Glitches, and the Autism Explosion

Slides from Society for Neuroscience Wonder, February 2017

This presentation to a student-run chapter of SFN explained the history and science behind the “Time Bomb” hypothesis of autism.

DES DiEthylStilbestrol Resources

Autism outcomes in DES grandchildren : support the first study !

Help Fund Research into Neurodevelopment and Behavioral Impacts of DES

” My name is Jill Escher. I’m a science philanthropist who kickstarts pioneering research projects investigating the generational toxicity of certain potent exposures, including DES, tobacco and other drugs. While I’m not a DES daughter, I was exposed to a multitude of other synthetic steroid hormones in utero as part of a then-popular, if ineffective, “anti-miscarriage” practice. You can read my story here. You can see my science website at

Based on human, animal, and in vitro studies, as well as family interviews, I hypothesize that diethylstilbestrol DES, along with several other toxic substances, can damage the genomic information in early fetal-stage gametes. For a variety of reasons, the early gamete is probably the single most vulnerable stage of the human lifecycle. Damage during that phase, which could be genetic or epigenetic in nature, can manifest as abnormal development in the subsequent offspring.

For example, I hypothesize that the intensive synthetic steroid hormone drug regimen to which I was subjected as a fetus subtly deranged the molecular programming of my early eggs. This derangement I believe resulted in the starkly abnormal neurodevelopment — autism — of my children. I have met many other families with the same story.

Support Research into the Far-Reaching Generational Toxicity of DES, germline exposures, 10/10/2016.

Autism by pycik.

I am pleased to announce that I am funding the world’s first research study into the grandchild effects of DES (3d gen), looking specifically at neurodevelopment and behavioral impacts. This work will be done in collaboration with Harvard University, based on the Nurses’ Health Study II.

Thank you for your support! If you have any questions, please do not hesitate to email me. “

Jill Escher, President of Autism Society San Francisco Bay Area, 10/10/2016.

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Old Exposures, Heritable Effects, and Emerging Concepts for Autism Research

Out of the past – heritable effects of endocrine disruptors

Video published on 27 May 2016 by FSUMedMedia channel.

Presentation given by Jill Escher on April 8, 2016 at Florida State University’s Symposium on the Developing Brain.

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Out of the Past

Old Exposures, Heritable Effects, and Emerging Concepts for Autism Research

The presentation highlights a significant gap in autism research: what factors might be driving the heterogenous de novo genomic errors seen in autism?

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Multigenerational Effects of Endocrine-Disrupting Molecules

Emilie Rissman PhD, interviewed by Jill Escher, 2014

rippled-reflections image
I would stress that our data show that in mice, social interactions, as a class of behaviors, are disrupted by transgenerational exposure to ‘human-like’ levels of BPA. ” Rippled reflections by 57Andrew.

Emilie Rissman, PhD, Professor of Biochemistry & Molecular Genetics, University of Virginia, studies mammalian behavioral genetics. Because many social behaviors are activated only when gonadal steroid hormones are present, the genes for steroid hormone receptors are currently under study in her lab. She has found that androgen receptor is required for normal social affiliative behavior in male mice. In addition, her work shows that several social behaviors are sexually dimorphic, in part, because of differences in sex chromosome genes. Her work in mice is relevant to several sexually dimorphic neurobehavioral diseases including autism spectrum disorder.

  • Dr. Rissman, I’m very pleased to be interviewing you because since you are one of the few researchers to explicitly examine multigenerational effects of endocrine disruption as it relates to abnormal behavior and neurodevelopment in offspring. How did you come to examine this question?
  • How did gestational BPA exposure differentially affect succeeding generations?
  • What epigenetic mechanisms are at play with exposure to EDCs?
  • What do we know about hormone and other receptors on and in germ cells? And somatic cells, if there’s a difference.
  • What role does the steroid hormone receptor play in epigenetic function?
  • Why do hormone-disrupting molecules affect epigenetic activity?
  • Some of the scientists I’ve spoken with differentiated between “strong” exposures and weak ones in terms of likelihood of epigenetic impacts. Some strong ones mentioned included steroid hormones and their mimics, cigarette smoke and psychoactive drugs. Comparatively weak ones were thought to include variability in stress and nutrition. Do you agree with this general distinction?
  • It seems we forget there’s a long and complicated molecular phase of the human life cycle. For example, those who say BPA or pesticides are safe cite studies on adults, children or fetuses. But isn’t the most vulnerable phase gametes and precursor cells? What do you consider to be important windows of vulnerability?
    While nearly all scientists find endocrine disruption a concern, some say “there’s just not enough evidence yet” to be concerned about ambient exposures. How do you respond to that? What would be “enough” evidence?

Read the full interview on Germline Exposures, by Jill Escher, April 2014

The 8th Annual Autism Spectrum Disorders Update

Connecting the Dots: Clinical Research for Autism. Making A difference for our Children

Lucile Packard Children’s Hospital Stanford is here to help parents find answers.
On April 18, 2015 the Stanford Autism Center at Packard Children’s Hospital presents its 8th Annual Autism Spectrum Disorders Update, an event that gives members of the community a chance to learn about new autism research and therapies.

Lucile Packard Children's Hospital Stanford banner image
Jill Escher will be speaking on the exploding autism numbers at the Stanford Autism Conference in April. See you there?

Connecting the Dots: Clinical Research for Autism. Making A difference for our Children

  • REGISTRATION FEE: The registration fee is $125.00. The fee includes a continental breakfast, buffet lunch and speaker handouts.
  • WHERE: McCaw Hall in the Francis C. Arrillaga Alumni Center. 326 Galvez Street, Stanford, California 94035.
  • Parking is free and located at Galvez Field on the corner of Galvez Street and Campus Drive East.
  • WHEN: April 18, 2015 from 8:15 a.m. to 4:30 p.m. (Registration and continental breakfast begin at 7:30 am).
  • WHO SHOULD ATTEND: Parents, teachers, pediatricians, psychologists, caregivers, media and anyone with an interest in autism are invited to attend.
  • CONTACT: For further information, please contact the Stanford Autism Center at Packard Children’s Hospital at (650) 721-6327 or e-mail Maura Chatwell.
Sources and more information
  • I will be speaking on the exploding #autism numbers at the Stanford Autism Conference in April. See you there? Jill Escher.
  • The 8th Annual Autism Spectrum Disorders Update, stanford childrens.

Epigenetics and the Multigenerational Effects of Nutrition, Chemicals and Drugs

Video published on 11 Aug 2014 by AncestryFoundation

Speaker Jill Escher, mother of two children with autism, will also share her experience as a member of the “guinea pig generation” heavily exposed in utero to novel synthetic drugs popular in the 1960s. Learn more about the work of the Escher Fund at Germline Exposures.

  • By now most of us know gene expression can be upregulated or downregulated by molecular factors including the metabolites of drugs, chemicals and nutrition. But what are the implications of this environmentally labile landscape, not only for our somatic (body) cells, but also our germ cells, which contain our genetic and epigenetic molecules of inheritance? In this presentation by a science philanthropist (Escher Fund for Autism) who focuses on cutting-edge gene-environment interaction research, you will learn: • How genes respond to environmental cues.
    •  How evolutionary concepts are broadening to include environmental responsivity of genes and the germline.
    •  How, from a biological point of view, the human lifecycle begins about 20-40 years before conception with the dynamic, complex, and lengthy molecular phase of germline (egg and sperm) development.
    •  How, in light of the true breadth of the human lifecycle, risks of exposures are routinely underestimated.
    •  How ancestral health principles are critical to reducing pervasive and serious risks, and improve health across the generations.
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An Autism Mom on a Mission

by Jane Kay, feat. Jill Escher “Autism Exposed” interview

An Autism Mom on a Mission
Jill Escher, Autism science and programs philanthropist, autism mom, businesswoman, author

Three years ago, Jill Escher had an epiphany, one that now consumes her waking hours and night time dreams. After prodding her mother for clues from her past, Jill discovered some hidden history: Her mother had sought help conceiving at a fertility clinic. As she grew in her mother’s womb, Jill was bombarded with synthetic hormones and other drugs.

Now Jill Escher‘s dogged quest to unravel why this happened to her children has drawn the attention of scientists, and may ultimately lead to a greater understanding of how prescription drugs — and perhaps chemicals in the environment — may secretly and subtly harm the health of generations to come. ”

  • From generation to generation
  • A personal quest
  • Critical exposure
  • More research needed
  • Family histories
  • Antidepressants under the scope

Read Mom on a Mission
by Jane Kay, 1 Oct 2013, feat. Jill Autism Exposed interview