Common Autism Spectrum Disorder Causes You Should Know

Recent studies highlight key autism spectrum disorder causes spanning genetics, prenatal health, and environmental exposures. Families, educators, and clinicians often seek clarity on what drives ASD risk, given its rising prevalence. This article provides a clear overview of well-documented risk factors linked to autism so that they can grasp underlying mechanisms and consider early support strategies.
By examining maternal health conditions, hormonal influences, genetic contributions, and environmental toxicants, readers will gain a concise yet thorough understanding of common factors associated with ASD risk.
Maternal Health Conditions
Maternal health covers a range of conditions, but what does obesity or diabetes have to do with ASD risk? Evidence shows that metabolic disorders and infections during pregnancy can increase the likelihood of autism in offspring.
Diabetes and Obesity
Pregnant individuals with pre-existing type 2 diabetes, gestational diabetes, or obesity face higher odds of having a child later diagnosed with autism spectrum disorder. The table below summarizes reported increases in ASD odds:
Maternal Factor | Increased ASD Odds |
---|---|
Type 2 Diabetes | 1.3-fold |
Gestational Diabetes | 1.5–1.7-fold |
Pre-pregnancy Obesity | 1.3–2.0-fold |
Excess Weight Gain | 1.1–1.6-fold |
These patterns likely reflect disruptions in inflammatory pathways, hormone metabolism, and glucose regulation. Close monitoring and early interventions may help mitigate risks.
Infections and Fever
Maternal immune activation is another factor under scrutiny. A large Danish study linked viral infections during pregnancy to a 2.8-fold increase in ASD risk, while bacterial infections carried a 1.4-fold rise. Overall, any fever or infection seemed to boost autism odds by about 1.3-fold. Prompt management of infections and fever in expectant parents remains essential.
Prenatal Hormonal Influences
Hormone levels shape early brain wiring, and imbalances can contribute to neurodevelopmental changes associated with autism.
Progesterone and Progestin Exposure
Some studies suggest that prenatal exposure to progestin-contaminated seafood or supplemental progesterone may alter hormone receptors in the developing brain, potentially elevating ASD risk. While findings are mixed, this underscores the importance of carefully weighing the benefits and risks of hormonal treatments in pregnancy.
PCOS and Hormone Imbalances
Polycystic ovary syndrome (PCOS) affects up to 10 percent of women of childbearing age and is linked to altered androgen levels. Research indicates that maternal PCOS correlates with an increased autism prevalence in children, possibly due to excess prenatal androgens influencing brain differentiation.
Genetic Contributions to ASD
What role do genes play in autism spectrum disorder? Genetics accounts for an estimated
40–80 percent of ASD risk, reflecting both common and rare variants.
Heritability and Gene Variants
Twin studies show high concordance rates in monozygotic twins, confirming a strong genetic component. Dozens of common gene variations, mostly affecting synapse formation, neurotransmitter function, and neuronal growth, each exert a small individual effect. Still, collectively they shape the neurodevelopmental trajectory.
Copy Number Variations
Submicroscopic structural changes in chromosomes, known as copy number variations (CNVs), contribute directly to about 10 percent of ASD cases. Deletions or duplications in regions like 16p11.2 can disrupt genes critical for neuronal connectivity.
Genetic Factor | ASD Contribution |
---|---|
Common Variants | Small individual effects, high prevalence |
Rare Mutations | 2–4 percent of cases (ADNP, CHD8, PTEN) |
CNVs | ~10 percent of cases |
Environmental Toxicants Impact
Environmental exposures can intersect with genetic susceptibility, adding to ASD risk. Which toxicants stand out?
Air Pollutants and Pesticides
Inhaling particulate matter and pesticide residues during pregnancy has been associated with higher autism spectrum disorder. Multiple studies report that near-roadway air pollution and agricultural pesticide use correlate with up to 1.5-fold increases in ASD risk.
Heavy Metals and Phthalates
Exposure to lead, mercury, and phthalates can disrupt endocrine function and neurodevelopment. While some biomarker studies show elevated concentrations in children with autism, findings remain mixed. Overall, 92 percent of environmental exposure studies link these agents to ASD risk.
Prenatal Medications
Certain medications taken during pregnancy may also influence ASD odds. Use of selective serotonin reuptake inhibitors (SSRIs) in the first trimester has been tied to a 1.5–4.5-fold increased risk, while antibiotics show a modest 1.1–1.5-fold rise. Medication decisions should balance maternal needs with potential long-term effects.
Neurotransmitter and Brain Changes
Early alterations in brain chemistry and growth patterns appear central to autism spectrum disorder causes.
Early Cortical Growth Patterns
Infants later diagnosed with ASD show rapid cortical surface area expansion between 6–12 months, followed by brain volume overgrowth at 12–24 months. These changes often precede behavioral symptoms and may signal atypical neural connectivity.
Neurotransmitter Dysregulation
Studies identify imbalances in gamma aminobutyric acid (GABA) and glutamate systems in autism, affecting information processing. Abnormal GABA-glutamate ratios in regions like the striatum may underlie sensory and social symptoms.
Interactions Between Genes and Environment
Autism risk emerges from complex gene-environment interplay. Epigenetic modifications, such as changes in gene expression without altering DNA sequence, can result from toxicant exposure, infections, or metabolic stress. For example, polymorphisms in detoxification genes (GSTM1, GSTP1, PON1) heighten sensitivity to pollutants, further increasing ASD likelihood in certain populations. Recognizing these interactions is key to targeted prevention and personalized support.
Conclusion
A range of factors contribute to autism spectrum disorder causes, from maternal health and hormonal shifts to genetic mutations, environmental toxicants, and early brain changes. While no single cause explains every case, understanding these common risk elements empowers families and professionals to support early identification and tailored interventions. Ongoing research continues to refine risk estimates and clarify mechanisms, guiding best practices in prenatal care, environmental safety, and early developmental screening. As insights evolve, multidisciplinary collaboration remains essential to help individuals with ASD thrive.
While research continues to explore the many factors that contribute to autism, one thing is certain—early, personalized intervention makes a difference. At Achieve Behavioral Therapy, we provide compassionate, evidence-based ABA therapy for children with autism across New Jersey and North Carolina. Our BCBAs and RBTs partner with families to create individualized plans that help children build communication, social, and daily living skills.
Contact us today to learn how our ABA services can support your child’s growth and development.
Frequently Asked Questions
What causes autism?
Autism has no single cause. It is influenced by a combination of factors, including genetics, prenatal conditions, early brain development, and possible environmental contributors.
Can autism be prevented?
No. Autism cannot be prevented, but early detection and intervention can greatly improve outcomes by addressing developmental challenges early in life.
Does early intervention help children with autism?
Yes. Evidence shows that early intervention, especially ABA therapy, can significantly improve communication, social skills, and adaptive behaviors, giving children the best chance to thrive.
SOURCES:
https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-024-03617-3
https://pmc.ncbi.nlm.nih.gov/articles/PMC8902545/
https://medlineplus.gov/genetics/condition/autism-spectrum-disorder/
https://pmc.ncbi.nlm.nih.gov/articles/PMC6710438/
https://pmc.ncbi.nlm.nih.gov/articles/PMC3944636/
https://pmc.ncbi.nlm.nih.gov/articles/PMC5336143/
https://pmc.ncbi.nlm.nih.gov/articles/PMC7139720/
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