Understanding what happens before birth is foundational for school psychologists, child and adolescent counselors, pediatric clinicians, and anyone working with families — because the prenatal environment shapes neurological structure, behavioral temperament, and developmental risk in ways that extend throughout childhood and beyond. PSY6010 brings together embryology, neuroscience, epigenetics, and clinical practice.
Stages of prenatal development
Prenatal development is conventionally divided into three stages, each characterized by different biological events and different windows of vulnerability to environmental disruption:
- Germinal stage (weeks 0–2): Fertilization of the ovum by a spermatozoon forms a zygote with 46 chromosomes (23 pairs). The zygote undergoes rapid mitotic cell division (cleavage) while traveling down the fallopian tube. By day 4, the morula (a solid ball of cells) has formed; by day 5–6, the blastocyst (a hollow sphere) has developed, with the inner cell mass (ICM) that will become the embryo and the outer trophoblast that will become the placenta. Implantation of the blastocyst in the uterine wall occurs at approximately day 6–10. Approximately 50–60% of fertilized eggs fail to implant — the majority lost before pregnancy is recognized.
- Embryonic stage (weeks 3–8): The ICM differentiates into three germ layers — ectoderm (skin, nervous system, sense organs), mesoderm (muscles, skeleton, circulatory system, kidneys), and endoderm (digestive tract, lungs, liver) — through the process of gastrulation. The neural plate forms from the ectoderm by week 3 and folds into the neural tube by week 4 — the beginning of the central nervous system. By week 8, all major organ systems are established (organogenesis is complete); the organism has a recognizable human form at about 3 cm and 3 grams. This period is the most critical for teratogenic effects — disruption during organogenesis can produce severe malformations.
- Fetal stage (weeks 9–birth): Growth and maturation of systems established in the embryonic stage. The brain undergoes dramatic development — neurogenesis (production of neurons) peaks between weeks 10–20, producing approximately 250,000 neurons per minute at its peak. Migration of neurons to their final cortical positions and synaptogenesis (formation of synaptic connections) occur throughout the fetal period and continue postnatally. The fetus reaches viability (ability to survive outside the womb with medical support) at approximately 22–24 weeks gestational age, though outcomes improve significantly after 28 weeks.
Teratology: environmental threats to prenatal development
Principles of teratology (Moore & Persaud)
- Susceptibility depends on developmental timing: The embryonic period (3–8 weeks) is most vulnerable to major structural malformations; the fetal period is more vulnerable to functional abnormalities (behavioral, cognitive, sensory) and growth disruption. The same teratogen can produce very different effects depending on the gestational week of exposure.
- Dose-response relationship: Teratogenic risk typically increases with dosage — low-level exposure may produce no detectable effect, while high-level exposure produces severe malformations. There may be threshold effects below which the teratogen produces no measurable harm.
- Genetic susceptibility: Both the pregnant person's and the embryo's genotype influence teratogenic risk. The same teratogenic exposure can produce different outcomes in genetically different embryos — explaining why not all exposed pregnancies result in the same pattern of defects.
- Major teratogens: Alcohol (Fetal Alcohol Spectrum Disorders — FASD — affecting 1–5% of U.S. children; the most common preventable cause of intellectual disability); tobacco (growth restriction, preterm birth, SIDS risk); illicit drugs (cocaine, methamphetamine, opioids — neonatal abstinence syndrome); medications (thalidomide historically; valproate, retinoids, ACE inhibitors with known teratogenicity); infections (TORCH: Toxoplasmosis, Other — syphilis, varicella — Rubella, Cytomegalovirus, Herpes; Zika virus causing microcephaly); radiation; environmental chemicals (lead, mercury, PCBs).
Prenatal brain development and the origins of behavior
The developing brain is remarkably behaviorally active before birth. Fetal movement begins by week 7–8 and is detectable by the pregnant parent by 16–20 weeks. Habituation — decreased responding to a repeated stimulus — has been demonstrated in the fetus as early as 22–23 weeks, suggesting primitive learning capacity. Auditory processing is functional by 25–28 weeks; fetuses respond to sounds, including their parent's voice, and show preferences for familiar voices and language patterns postnatally — reflecting prenatal auditory experience. Prenatal stress and maternal cortisol are associated with altered fetal behavioral reactivity, providing a mechanism for transgenerational stress transmission.
Epigenetics and prenatal programming
Epigenetics — heritable changes in gene expression that do not involve changes in DNA sequence — has transformed our understanding of how prenatal experience shapes development. Maternal nutrition, stress, substance exposure, and toxic environmental chemicals can alter DNA methylation and histone modification patterns that affect gene expression in ways that persist throughout the child's lifetime and may even be transmitted to subsequent generations. The Developmental Origins of Health and Disease (DOHaD) hypothesis (Barker, 1990s) proposes that prenatal nutritional insufficiency programs the fetus for a "thrifty phenotype" that increases later risk of metabolic syndrome, cardiovascular disease, and type 2 diabetes.
PSY6010 assignments include teratology case analyses, prenatal brain development papers, and prenatal risk research reviews
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Frequently asked questions
Fetal alcohol spectrum disorder (FASD) is an umbrella term for a range of conditions caused by prenatal alcohol exposure. Alcohol is a teratogen that crosses the placental barrier freely; there is no known safe amount of alcohol at any gestational stage, though the effects are most severe with heavy, chronic exposure during the first trimester. FASD encompasses Fetal Alcohol Syndrome (FAS) — the most severe form, characterized by facial dysmorphology (flat philtrum, thin upper lip, small palpebral fissures), prenatal and postnatal growth deficiency, and central nervous system dysfunction (intellectual disability, attention and memory deficits, behavioral dysregulation) — as well as partial FAS, alcohol-related neurodevelopmental disorder (ARND), and alcohol-related birth defects (ARBD). FASD is estimated to affect 2–5% of school-age children in the U.S. (Chasnoff et al., 2010; May et al., 2018), making it the most common preventable cause of intellectual disability and neurodevelopmental disorder. In educational and mental health practice, FASD is frequently undiagnosed or misdiagnosed as ADHD, oppositional defiant disorder, or learning disability — because the facial features may be subtle and many practitioners are not trained to screen for it. Practitioners who complete PSY6010 learn to recognize FASD risk indicators and make appropriate referrals for comprehensive FASD evaluation.