What Increases the Risk of Autism in Pregnancy?

Several factors during pregnancy are linked to a higher likelihood of autism in offspring, ranging from metabolic conditions like obesity and diabetes to infections, certain medications, and environmental exposures. Genetics still accounts for the largest share of autism risk, with heritability estimates between 40% and 80%, but the environmental and prenatal factors are increasingly well documented and, in many cases, modifiable.

Maternal Obesity and Diabetes

Metabolic health before and during pregnancy is one of the most consistently studied risk factors. Mothers with a pre-pregnancy BMI of 30 or higher have roughly double the odds of having a child with autism compared to mothers at a normal weight. Diabetes adds its own layer of risk: mothers with any form of diabetes have about a 62% higher chance of having a child later diagnosed with autism.

The combination of obesity and diabetes raises the risk further. Women with pre-existing diabetes and severe obesity face up to a six-fold increase in risk compared to mothers of normal weight without diabetes. Gestational diabetes diagnosed around 26 weeks of pregnancy has been associated with a 42% increase in autism risk on its own. The risk appears to be even higher when the child is male, which aligns with the broader pattern of autism being diagnosed more frequently in boys.

The biological explanation centers on inflammation and altered nutrient signaling. Elevated blood sugar and certain amino acid levels can cross the placenta and affect how the fetal brain develops during critical windows of growth.

Infections and Fever During Pregnancy

The mother’s immune response during pregnancy can influence fetal brain development, and severe infections appear to be a meaningful risk factor. A large Danish study covering children born between 1980 and 2005 found a nearly threefold increase in autism risk following hospitalization for a viral infection in the first trimester and an elevated risk after bacterial infections requiring hospitalization in the second trimester. Infections diagnosed in outpatient settings, which tend to be milder, did not carry the same association.

Fever itself plays a role. Influenza exposure during pregnancy has been linked to a roughly twofold risk of autism, and fevers lasting longer than one week were tied to a nearly threefold increase. One study from Kaiser Permanente Northern California found that fever during pregnancy was more strongly associated with autism when the mother did not take anti-fever medication, suggesting that the intensity and duration of the immune response matter more than the specific infection.

Valproate and Other Medications

Valproate, an anti-seizure medication sometimes used for epilepsy or bipolar disorder, carries one of the most clearly documented medication-related risks. Children exposed to valproate in the womb had an absolute risk of 4.4% for autism spectrum disorder, roughly triple the rate seen with other anti-epileptic medications. The risk held even among children whose mothers did not have epilepsy. Other anti-seizure medications, including carbamazepine and lamotrigine, were not associated with the same increase.

Antidepressants in the SSRI class have also been studied. A meta-analysis pooling seven studies found that prenatal SSRI exposure was associated with an 82% increase in autism odds, even after adjusting for the mother’s depression. However, this finding comes with caveats: many of the included studies did not account for the use of other psychiatric medications alongside SSRIs, and maternal depression itself may independently affect fetal development. The question of whether it’s the medication or the underlying condition driving the risk remains unresolved.

Air Pollution Exposure

Prenatal exposure to fine particulate matter, specifically certain chemical components of PM2.5, has been linked to autism risk in a large cohort study published in JAMA Network Open. Exposure to sulfate and ammonium particles during the second and third trimesters showed a 12% to 15% increase in risk per unit increase in concentration. Ozone exposure during the first year of life was also associated with a 9% increase in autism risk.

These effect sizes are modest on an individual level, but because air pollution exposure is so widespread, the population-level impact could be significant. Living near major roadways or in areas with high industrial emissions increases exposure to these specific components.

Short Intervals Between Pregnancies

Conceiving again less than 12 months after a previous birth is associated with roughly double the risk of autism in the next child, compared to spacing pregnancies 24 to 47 months apart. This finding has been replicated across studies in California, Norway, and other populations. One plausible explanation is nutritional depletion: pregnancy draws heavily on folate, iron, and other nutrients, and the body may not fully replenish these stores within a short window. Interestingly, very long intervals (more than 84 months) also showed a twofold increase, suggesting a U-shaped relationship.

Preterm Birth and Low Birth Weight

Babies born very early or very small face elevated odds of an autism diagnosis later in childhood. Infants born before 32 weeks of gestation are about two and a half times more likely to be diagnosed with autism compared to full-term infants. Very low birth weight babies, those under about 3.3 pounds, have more than triple the odds. Even babies born at term but small for their gestational age carry a 70% increased risk.

These are not causes in the traditional sense. Preterm birth and low birth weight are often the result of other underlying factors, including infection, placental problems, and maternal health conditions. But the premature transition from womb to outside world may itself disrupt brain development during a period when neural connections are forming rapidly.

Folic Acid as a Protective Factor

Not all prenatal factors increase risk. Folic acid supplementation during early pregnancy is one of the most consistent protective findings in the research. A meta-analysis found that taking at least 400 micrograms of folic acid daily, the amount in most standard prenatal vitamins, was associated with a 45% reduction in autism risk. The protective window appears to be early pregnancy, ideally starting before conception and continuing through the first trimester, which is also the period when folic acid protects against neural tube defects.

This is one of the most actionable findings in the field. Because many pregnancies are unplanned, taking folic acid regularly during reproductive years provides a buffer even before a pregnancy is confirmed.

Parental Age

Both advanced maternal and paternal age have been linked to increased autism risk in multiple large studies. The association is stronger for fathers, with risk rising notably after age 40. Older paternal age is thought to contribute through an accumulation of new genetic mutations in sperm over time. Maternal age over 35 also carries a modest increase, though the mechanisms are less well understood and may overlap with higher rates of pregnancy complications in older mothers.

How These Factors Work Together

No single factor on this list “causes” autism in isolation. Autism arises from a combination of genetic predisposition and environmental exposures, and the relative contribution of each varies from person to person. Heritability estimates for autism range from 40% to 80%, meaning genetics plays a large role, but it leaves substantial room for prenatal and environmental influences to tip the balance.

Many of these risk factors share overlapping biological pathways. Obesity, diabetes, infection, and air pollution all trigger inflammatory responses that can cross the placenta and affect the developing brain. Nutritional deficiencies, whether from poor diet, short pregnancy intervals, or lack of supplementation, may leave the fetal nervous system more vulnerable to these insults. The risks are cumulative, not singular, and they interact with each child’s unique genetic makeup in ways that are still being mapped out.