Introduction

Autism is not a single story or a single cause. It’s a spectrum influenced by many factors—genetic, prenatal, and perinatal—that interact with timing and context during early brain development. My goal with this article is straightforward: to cut through noise, share what science supports, and offer practical guidance you can use now—care, clarity, compassion. 

The big picture

• There is no single cause. Most autism risk results from polygenic influences—many common gene variants cumulatively contribute. A smaller proportion involves rare variants and CNVs (such as CHD8, SCN2A, SHANK3, 16p11.2) with varying effects. [11] [3]
• Timing matters. Influences before birth and around delivery carry the most weight.
• Environmental factors ≠ blame. In science, “environmental” often refers to factors like advanced parental age, prematurity, pregnancy complications, significant maternal infection/fever, or certain medications (e.g., valproate)—not parenting style.
• Heterogeneity is the rule. Two autistic individuals can receive the same diagnosis but have completely different strengths, challenges, and developmental backgrounds. That diversity is genuine—and significant.

Myths we can retire

• “Refrigerator mother”: The mid-20th-century idea that distant parenting “caused” autism has been thoroughly disproved. Autism is a neurodevelopmental condition with strong genetic roots.
• “Vaccines cause autism”: They do not. A small, flawed 1998 study fueled a lasting myth; it was retracted, the author lost his medical license, and large, high-quality studies worldwide have found no link. Vaccines protect children’s health and do not cause autism. [9] [4–6]

What remains uncertain—and where evidence is converging

Science is transitioning from “one culprit” thinking to multi-pathway models. Questions we’re currently studying:

• Which gene–environment combinations are relevant for different individuals? For example, how high polygenic risk or a rare variant might interact with maternal fever/inflammation, extreme prematurity, air pollution (PM2.5), severe prenatal stress, or periconceptional folate status to influence the likelihood. [8]
• How to translate risk into earlier support. We’re combining genetics with early neurodevelopmental markers—such as social attention trajectories, language timing, EEG signatures, and subtle motor patterns—to identify needs sooner and tailor supports.

Practical guidance for pregnancy

• Acetaminophen (Tylenol): Current evidence shows no proven causal link between acetaminophen use during pregnancy and autism. Some observational studies report small, inconsistent associations, but these are vulnerable to confounding factors, including the reason for the medication, recall bias, genetics, and co-exposures. [1–2, 10]
• Treat fever and significant pain (untreated fever carries risks)
• Use the lowest effective dose for the shortest time
• Avoid stacking combination products; read labels
• Discuss the potential risks of frequent or prolonged use with your obstetrician or clinician
• General prenatal health:
• Keep vaccinations and prenatal care up to date
• Take prenatal vitamins, including folate, as recommended
• Manage chronic conditions; seek care for significant infections or fever
• Prioritize sleep, nutrition, movement, and stress-reduction techniques (such as breathwork, mindfulness, and gentle yoga as approved)

Guidance for parents of infants and toddlers

• Watch the “communication triangle”: shared gaze, back-and-forth sounds, and pointing. Every child develops on a unique timetable, but if these behaviors are consistently limited, it’s worth taking a closer look.
• Trust your observations. If you’re worried about language, social responses, or repetitive behaviors, talk to your pediatrician about a developmental screening or referral for an evaluation.
• Start support early, whether a diagnosis has been made or not. You don’t need to wait to begin parent-mediated coaching, language scaffolding, sensory and sleep strategies, or occupational or speech therapy if recommended.
• Co-occurring conditions are important. ADHD, anxiety, sleep disorders, epilepsy, and GI issues are common and treatable. Addressing them often leads to progress.

How to think about “risk”

Risk ≠ destiny. Family history, genetic variants, prematurity, or prenatal exposures indicate probability, not a verdict. Many children with “higher risk” never meet diagnostic criteria, and those who do have widely varying outcomes. We use risk to guide monitoring and early support, not to label or limit a child’s potential.

At MindClaire, we focus on function and quality of life over labels. Care is collaborative and practical:

• For children: parent-coaching models, language and play-based interventions, AAC when helpful, sensory-smart routines, sleep hygiene, and school plans (IEP/504).
• For teens: executive-function coaching, anxiety management, social skills in real contexts, and transition planning.
• For adults: workplace accommodations, energy and sensory management, sleep and mood care, and community supports.
• For families: psychoeducation, stress-reduction tools, and a compassionate space for questions—because guidance works best when it’s human.

What to do next (a simple action plan)

1. If you’re pregnant, follow standard prenatal care, treat fevers, use acetaminophen carefully, and discuss any frequent medication use with your doctor.
2. If you have developmental concerns, request screening and pursue early-intervention services where appropriate — earlier is better, but it’s never too late.
3. Build the team: pediatrician, developmental specialist, speech/OT, school services, and—when helpful—child and adolescent psychiatry for co-occurring challenges.
4. Protect sleep and routines: small, steady changes compound.
5. Keep expectations flexible: your child’s profile is unique, so support should be as well

About the author

Ritu Goel, MD, DFAACAP, is a double board-certified Child, Adolescent & Adult Psychiatrist and Distinguished Fellow of the American Academy of Child & Adolescent Psychiatry. She serves as a Principal Investigator and chairs pediatric Data Monitoring Committees for autism clinical trials. Her work centers on translating complex evidence into practical, family-centered guidance.

References

1. American College of Obstetricians and Gynecologists. (2025, September 22). Acetaminophen use in pregnancy and neurodevelopmental outcomes (Practice Advisory). https://www.acog.org/clinical/clinical-guidance/practice-advisory/articles/2025/09/acetaminophen-use-in-pregnancy-and-neurodevelopmental-outcomes
2. American College of Obstetricians and Gynecologists. (n.d.). Acetaminophen and pregnancy (FAQ). Retrieved October 2, 2025, from https://www.acog.org/womens-health/faqs/acetaminophen-and-pregnancy
3. Bernier, R., Golzio, C., Xiong, B., Stessman, H. A., Coe, B. P., Penn, O., … Eichler, E. E. (2014). Disruptive CHD8 mutations define a subtype of autism early in development. Cell, 158(2), 263–276. https://doi.org/10.1016/j.cell.2014.06.017
4. Hviid, A., Hansen, J. V., Frisch, M., & Melbye, M. (2019). Measles, mumps, rubella vaccination and autism: A nationwide cohort study. Annals of Internal Medicine, 170(8), 513–520. https://doi.org/10.7326/M18-2101
5. Jain, A., Marshall, J., Buikema, A., Bancroft, T., Kelly, J. P., & Newschaffer, C. J. (2015). Autism occurrence by MMR vaccine status among US children with older siblings with and without autism. JAMA, 313(15), 1534–1540. https://doi.org/10.1001/jama.2015.3077
6. Madsen, K. M., Hviid, A., Vestergaard, M., Schendel, D., Wohlfahrt, J., Thorsen, P., … Melbye, M. (2002). A population-based study of measles, mumps, and rubella vaccination and autism. New England Journal of Medicine, 347(19), 1477–1482. https://doi.org/10.1056/NEJMoa021134
7. Sandin, S., Lichtenstein, P., Kuja-Halkola, R., Larsson, H., Hultman, C. M., & Reichenberg, A. (2017). The heritability of autism spectrum disorder. JAMA, 318(12), 1182–1184. https://doi.org/10.1001/jama.2017.12141
8. Surén, P., Roth, C., Bresnahan, M., Haugen, M., Hornig, M., Hirtz, D., … Stoltenberg, C. (2013). Association between maternal use of folic acid supplements and risk of autism spectrum disorders in children. JAMA, 309(6), 570–577. https://doi.org/10.1001/jama.2012.155925
9. The Editors of The Lancet. (2010). Retraction—Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. The Lancet, 375(9713), 445. https://doi.org/10.1016/S0140-6736(10)60175-4
10. U.S. Food and Drug Administration. (2025, September 22). FDA responds to evidence of possible association between autism and acetaminophen use during pregnancy (Press release). https://www.fda.gov/news-events/press-announcements/fda-responds-evidence-possible-association-between-autism-and-acetaminophen-use-during-pregnancy
11. Grove, J., Ripke, S., Als, T. D., Mattheisen, M., Walters, R. K., Won, H., … Børglum, A. D. (2019). Identification of common genetic risk variants for autism spectrum disorder. Nature Genetics, 51(3), 431–444. https://doi.org/10.1038/s41588-019-0344-8