Fact check: A mother's stress during pregnancy can influence the gender of her child

1. Why the claim that “stress changes your baby’s sex” grabbed headlines

Several cohort studies reported an association between higher maternal cortisol or stress markers and a greater probability of female births, creating headlines that maternal stress can influence sex ratios. The most-cited findings observed higher hair or salivary cortisol in women who later delivered girls and reported roughly doubled odds of a female birth in some samples, presenting a biologically plausible hypothesis that stress-related hormones might affect sperm/embryo survival or implantation ^{[1] [3]}. These studies are observational, use biomarkers and self-report, and stimulated interest because sex-ratio shifts are measurable at population scale.

2. Evidence that stress affects fetal growth — and differently by sex

Multiple studies show sex-specific effects of maternal psychological stress on newborn size, with some cohorts finding lower birthweight among girls and higher birthweight among boys when maternal stress is high, implying differential vulnerability or adaptive fetal responses by sex. This pattern is consistent across several publications reporting associations between prenatal stress and birth outcomes, and links to pathways such as inflammation and altered placental function have been proposed to account for these sex-specific differences in growth ^{[4] [5]}.

3. Newer triangulation and confounding analyses complicate simple causal claims

More recent work applying triangulation and control for confounding suggests that apparent effects of maternal stress on birth timing and weight are often reduced when socioeconomic factors, prior health, and measurement timing are accounted for, indicating the relationship is complex and not solely biological. One 2025 analysis emphasized that earlier associations with stress and neonatal outcomes are largely explained by confounders, underscoring that observational associations do not prove maternal stress directly determines fetal sex or health without careful causal inference ^[2].

4. Biological plausibility: hormones, timing, and differential vulnerability

Mechanistic arguments focus on stress hormones (cortisol), immune/inflammatory signaling, and placental responses as plausible mediators by which maternal stress could influence implantation, embryonic survival, or fetal development. Studies linking preconception cortisol with reduced odds of male birth and work on prenatal hormones and brain development provide a theoretical basis for sex differences, but mechanisms remain incompletely demonstrated in humans, and experimental evidence is absent, leaving room for alternative explanations such as measurement error, reverse causation, or unmeasured social determinants ^{[3] [1] [5]}.

5. Timing matters: preconception versus gestational exposure changes interpretation

Findings vary by when stress was measured. Some studies implicate stress around conception or preconception in shifting secondary sex ratios, while others focus on stress during specific gestational windows affecting growth. Literature reviews highlight that effects depend on exposure timing, which complicates generalized statements: a stressor before conception might plausibly affect conception dynamics, whereas mid- or late-gestation stress is more plausibly linked to growth and neurodevelopment rather than primary sex determination ^{[3] [6]}.

6. The limits of population studies: sample size, bias, and generalizability

Cohort studies differ in size, populations, and how stress is measured—hair or saliva cortisol, self-report instruments, or composite indices—leading to heterogeneity in results. Smaller or selective samples can overstate effects, and publication bias toward positive findings is possible. Triangulation studies that integrate multiple designs and better confounder control provide more conservative estimates, suggesting any real effect on sex ratio or outcomes is likely modest and context-dependent ^{[1] [2] [6]}.

7. What consumers and clinicians should take away for policy and practice

The best-supported, actionable inference is that maternal mental health matters for pregnancy outcomes, particularly for fetal growth and neurodevelopment risks mediated by inflammation and stress physiology, and addressing maternal stress remains a public-health priority. However, presenting maternal stress as a deterministic factor that changes a baby’s sex misstates the evidence: current research supports associations and plausible mechanisms but not definitive causation or population-wide predictive power ^{[5] [4]}.

8. Bottom line: strong signals, but no definitive cause-and-effect on sex

Collectively, studies from 2012 through 2025 document associations between maternal stress and both sex-specific neonatal outcomes and modest shifts in sex ratios in some cohorts, but more rigorous, triangulated research finds much of the signal attenuated after accounting for confounders. Therefore, the statement that a mother’s stress during pregnancy “can influence the gender of her child” is partially supported by observational associations but is overstated if presented as a causal or reliable effect, and any policy or personal decision-making should rely on the broader evidence about maternal mental health rather than presumed control over fetal sex ^{[1] [2] [3]}.