Pregnancy is governed by a shifting cascade of hormones, each appearing at a specific stage and performing functions that range from keeping the embryo alive in the first days to timing the onset of labor months later. Some of these hormones originate from the mother’s own glands, others from the placenta, and a few from the fetus itself. The interplay is remarkably precise, and when it goes wrong, it can explain complications from preterm birth to gestational diabetes. Understanding what each hormone actually does, and when, gives a much clearer picture of why pregnancy unfolds the way it does.
hCG and the First Weeks
Human chorionic gonadotropin, or hCG, is the hormone that home pregnancy tests detect. Its primary job in the earliest days is not diagnostic, though. The fertilized egg implants into the uterine lining, and the structure that released the egg from the ovary, called the corpus luteum, begins producing progesterone. Without a pregnancy, the corpus luteum would break down within about two weeks. hCG, secreted by the developing embryo and then the placenta, keeps the corpus luteum alive so that its progesterone output can sustain the pregnancy for roughly the next six to eight weeks, until the placenta matures enough to take over hormone production and the corpus luteum disappears.1PubMed Central. The inadequate corpus luteum
hCG levels rise steeply during the first trimester, roughly doubling every two to three days in early pregnancy, and then gradually taper off. This rapid rise is one reason morning sickness tends to peak around weeks eight to twelve. hCG also has a structural resemblance to thyroid-stimulating hormone, which means very high hCG levels can nudge the thyroid gland into mild overactivity. This condition, called gestational transient thyrotoxicosis, typically shows up as slightly elevated thyroid hormone and lower TSH in the first trimester, with mild or no symptoms.2PubMed. Pitfalls in the assessment of gestational transient thyrotoxicosis It usually resolves on its own as hCG levels decline after the first trimester.
Progesterone and Uterine Quiet
If hCG is the rescue signal, progesterone is the bodyguard. Its most critical role during pregnancy is keeping the uterus relaxed, a state researchers call “uterine quiescence.” The uterus is a muscular organ, and without progesterone actively suppressing it, it would contract. Progesterone achieves this through several mechanisms: it increases the activity of certain potassium channels in uterine muscle cells, dampening their electrical excitability; it reduces the levels of proteins that would otherwise trigger contractions; and it lowers the concentration of calcium signals that muscle cells use to contract.3PubMed Central. Effects of progesterone treatment on expression of genes involved in uterine quiescence Animal studies confirm the effect directly: progesterone causes concentration-dependent relaxation of uterine tissue even in late pregnancy.4PubMed Central. Progesterone inhibits contraction and increases TREK-1 potassium channel expression in late pregnant rat uterus
This is why progesterone supplementation is sometimes given to women at high risk of preterm birth. If the body does not produce enough on its own, or if the corpus luteum fails before the placenta is ready, the pregnancy can be jeopardized. Beyond the uterus, progesterone also plays a role in immune modulation during pregnancy, helping prevent the mother’s immune system from attacking the genetically distinct fetus.
Estrogens and Uteroplacental Blood Flow
Estrogen levels climb dramatically during pregnancy, reaching concentrations far higher than at any other point in a woman’s life. Three forms of estrogen matter here: estradiol, estrone, and estriol. Of these, estriol is the most pregnancy-specific. It originates almost entirely from the fetus: the fetal liver processes a precursor hormone, which is then converted by the placenta into estriol.5Clinical Research and Trials. Estriol review: Clinical applications and potential biomedical importance This means estriol levels in the mother’s blood partly reflect fetal well-being, which is why some prenatal screening tests measure it.
Estrogens collectively promote blood vessel growth and dilation in the uterus, increasing blood flow to the placenta. They also stimulate breast tissue development in preparation for lactation, raise levels of thyroid-binding globulin (which changes how thyroid tests are interpreted during pregnancy), and contribute to immune tolerance of the fetus.6PubMed. Immune-endocrine crosstalk during pregnancy In the breast specifically, estrogen and progesterone work together during pregnancy to grow the ductal system while simultaneously blocking milk secretion. Actual milk production does not begin until after delivery, when the sudden withdrawal of both hormones removes this brake and allows prolactin to take over.7PubMed. Lactation suppression
Metabolic Reshuffling by the Placenta
Growing a fetus is metabolically expensive, and the placenta secretes hormones that redirect nutrients from the mother to the baby. Two are especially important: human placental lactogen (hPL) and placental growth hormone (PGH).
hPL has been described in endocrine textbooks as a major driver of insulin resistance during pregnancy. The logic is straightforward: by making the mother’s cells slightly resistant to insulin, hPL spares glucose and amino acids so that more are available for the fetus. There is also evidence from animal and cell studies that hPL helps expand the insulin-producing beta cells in the mother’s pancreas, partly compensating for the resistance it creates.8PubMed Central. Human Placental Lactogen in Relation to Maternal Metabolic Health and Fetal Outcomes: A Systematic Review and Meta-Analysis In practice, though, directly linking hPL concentrations in an individual pregnant woman to her blood sugar control has turned out to be difficult. The relationship is real at a population level but messier than the textbook version suggests.
PGH does something unusual: it gradually replaces the mother’s own pituitary growth hormone during pregnancy. Rising PGH levels correlate with the mother’s insulin-like growth factor I (IGF-I) levels and with how fast the fetus is growing, particularly during the middle of pregnancy.9PubMed Central. Placental hormones, IGF-1, and early-life growth: endocrine links between birth size and infant metabolic programming—a systematic review In pregnancies where the feto-placental unit is not functioning well, PGH levels are low, and maternal IGF-I levels drop accordingly.10PubMed. Regulation of maternal insulin-like growth factor I by placental growth hormone in pregnancy. Possible action of maternal IGF-I on fetal growth The practical implication is that a poorly functioning placenta cannot adequately reprogram the mother’s metabolism, which can contribute to fetal growth restriction.
Relaxin and the Loosening Body
Many pregnant women notice that their joints feel looser, their feet seem to spread, or their pelvic area feels unstable. The hormone behind much of this is relaxin, produced primarily by the corpus luteum and later by the placenta and uterine lining. Relaxin alters the properties of cartilage and tendon by activating collagenase, an enzyme that breaks down collagen. It is also involved in bone remodeling and the healing of injured ligaments and skeletal muscle.11PubMed Central. The effect of relaxin on the musculoskeletal system
Relaxin’s loosening of the pelvic ligaments is an important preparation for delivery, widening the birth canal. But the effect is not limited to the pelvis, which is why some women experience pain in unexpected places like the wrists, knees, or lower back. The softening of connective tissue also contributes to the changes in foot size that many women notice during pregnancy, and those changes sometimes persist after delivery. In the cardiovascular system, relaxin promotes blood vessel dilation and helps increase cardiac output, though the details of how relaxin interacts with estradiol to influence cardiac output are still being worked out.12PubMed Central. Relationships between reproductive hormones and maternal pregnancy physiology in women conceiving with or without in vitro fertilization
The Placental Clock and the Onset of Labor
One of the more striking ideas in pregnancy endocrinology is that the timing of birth may be set far earlier in pregnancy than most people assume. The hormone at the center of this theory is corticotropin-releasing hormone (CRH), produced by the placenta in increasing amounts as pregnancy progresses. CRH has been proposed as part of a “placental clock,” where early activation of its production leads to preterm birth and later activation corresponds to term delivery.13PubMed Central. Preterm Birth and Corticotrophin-Releasing Hormone as a Placental Clock Elevated CRH in maternal blood at around 33 weeks has been linked not only to earlier delivery but also to fetal growth restriction, suggesting it plays roles in both the timing of labor and fetal maturation.14American Journal of Obstetrics & Gynecology. Maternal plasma corticotropin-releasing hormone associated with spontaneous preterm birth and fetal growth restriction
When labor actually begins, oxytocin takes center stage. Oxytocin drives rhythmic uterine contractions and is the hormone administered synthetically to induce or augment labor. But its role goes beyond direct muscle contraction. In the fetal membranes, oxytocin stimulates production of prostaglandins, which further promote cervical softening and uterine contractions.15PubMed Central. Labor and inflammation increase the expression of oxytocin receptor in human amnion The expression of oxytocin receptors in the uterus and membranes increases during labor, creating a positive feedback loop: the more contractions happen, the more receptive the tissue becomes to oxytocin, and the stronger the contractions get. This loop continues until delivery.
Immune Tolerance of the Fetus
The fetus carries half its genetic material from the father, making it immunologically foreign to the mother. Under normal circumstances, the immune system would attack tissue this genetically distinct. Pregnancy hormones are central to preventing that from happening. Estrogen, progesterone, and hCG all contribute to immune modulation, shifting the balance of the mother’s immune system toward tolerance rather than attack.16PubMed. Immune-endocrine crosstalk during pregnancy These hormones increase the number and activity of regulatory T cells, a class of immune cells that suppress immune responses against the fetus.17PubMed. The immunology of pregnancy: regulatory T cells control maternal immune tolerance toward the fetus
This immune suppression is not total. Pregnant women can still fight infections, though they may be more vulnerable to certain ones. The selective nature of the tolerance is remarkable: the immune system at the uterine lining learns to tolerate the specific fetal and placental cells without globally disabling infection defense. When this tolerance fails, the consequences can include recurrent miscarriage or complications like preeclampsia, where the mother’s immune system appears to respond abnormally to placental tissue.
Thyroid Demands in Pregnancy
Pregnancy increases thyroid hormone requirements substantially. Three things drive this: hCG’s mild stimulation of the thyroid (discussed above), a rise in thyroid-binding globulin driven by estrogen, and the fetus’s own need for thyroid hormone before its own gland starts functioning around mid-pregnancy.18PubMed Central. Thyroid hormone dysfunction during pregnancy: A review For most women, a healthy thyroid simply ramps up output. But for women with borderline thyroid function or existing thyroid disease, pregnancy can unmask problems. This is why thyroid function is monitored during prenatal care, and why women already on thyroid medication often need dose increases during pregnancy.
The Cortisol Barrier
Cortisol, the body’s primary stress hormone, rises considerably during pregnancy. Some of this is useful: cortisol helps regulate metabolism, supports fetal lung maturation in late pregnancy, and prepares the mother’s body for the metabolic demands of labor. But too much cortisol reaching the fetus can be harmful, potentially affecting fetal brain development and growth. The placenta handles this with a built-in enzymatic barrier. An enzyme called 11-beta-hydroxysteroid dehydrogenase type 2 converts active cortisol into an inactive form, effectively shielding the fetus from the mother’s higher cortisol levels.19PubMed. Placental 11beta-hydroxysteroid dehydrogenase type 2 is reduced in pregnancies complicated with idiopathic intrauterine growth Restriction
When this enzyme does not work well, the consequences are measurable. Pregnancies complicated by fetal growth restriction show reduced levels of this enzyme in the placenta. Severe maternal stress during pregnancy may also reduce the enzyme’s activity through changes in gene expression, potentially allowing more cortisol to cross to the fetus.20PLOS ONE. Epigenetic Effects of Prenatal Stress on 11β-Hydroxysteroid Dehydrogenase-2 in the Placenta and Fetal Brain This is one biological pathway through which maternal stress might affect fetal development, though the research is still working out how large the real-world effect is.
Leptin and Fat Storage
Leptin, a hormone produced mainly by fat tissue, rises substantially during pregnancy. The increase parallels a deliberate metabolic strategy: the body accumulates fat stores in the first two trimesters, then mobilizes those stores in the third trimester when fetal energy demands peak. Plasma leptin levels track this pattern, rising as fat is deposited and declining as it is burned off.21PubMed. Leptin levels in pregnancy: marker for fat accumulation and mobilization? The placenta also produces leptin, contributing to the elevated levels. This hormonal environment is one reason appetite changes during pregnancy do not simply reflect psychological factors; they are driven by genuine shifts in the hormones that regulate hunger and fat storage.
The Postpartum Hormone Crash
Delivery of the placenta eliminates the organ that was producing enormous quantities of estrogen, progesterone, hPL, PGH, and placental CRH. The result is one of the most dramatic hormonal shifts a human body ever experiences. Estradiol and progesterone concentrations plummet within hours of delivery. This rapid withdrawal has long been hypothesized to trigger postpartum depression in susceptible women.22PubMed Central. The role of reproductive hormones in postpartum depression Both hormones influence brain chemistry, including systems involved in mood, emotion, and cognition, and the speed of their decline after birth creates what researchers describe as a “vulnerable terrain.”23PubMed Central. THE NEUROENDOCRINOLOGICAL ASPECTS OF PREGNANCY AND POSTPARTUM DEPRESSION
Recent animal research has begun to identify specific brain pathways through which estrogen withdrawal may produce depressive symptoms, including receptors in a region called the lateral habenula that appears to mediate estrogen’s antidepressant effects.24PubMed Central. Estrogen receptor beta in lateral habenula mediates antidepressant effects of estrogen in postpartum-hormone-withdrawal-induced depression Not every woman who goes through this hormonal crash develops postpartum depression, which points to individual differences in how sensitive the brain is to these fluctuations. The hormonal shift is universal; the vulnerability is not.
Endocrine Disruptors and Pregnancy Hormones
Certain chemicals in the environment can interfere with the placenta’s hormone production. These endocrine-disrupting chemicals, found in some plastics, pesticides, and personal-care products, affect processes including how the placenta synthesizes steroid hormones, how it remodels blood vessels, and how it controls what substances cross from mother to fetus.25PubMed Central. Placenta Disrupted: Endocrine Disrupting Chemicals and Pregnancy The concern is that disrupting any part of the finely tuned hormonal cascade described above could have downstream consequences for both pregnancy outcomes and fetal development.
Researchers acknowledge that this is still a field with significant gaps. There is a lack of focused research on exactly how endocrine-disrupting compounds alter placental hormone production in living humans, as opposed to cell cultures or animal models.26PubMed Central. Models of Endocrine-Disrupting Effects: Human Placental Steroidogenesis What is known is enough to justify the precautionary advice many prenatal care providers give: minimize exposure to unnecessary chemicals during pregnancy where practical, without catastrophizing about everyday contact.
When the Father’s Hormones Change Too
Pregnancy hormones do not only affect the mother. Research on first-time expectant fathers has found that their hormone profiles begin shifting during their partner’s pregnancy. Testosterone and vasopressin levels are lower in expecting fathers compared to non-fathers, and these lower levels predict greater time spent with their partner and more positive engagement with the infant after birth.27PubMed Central. Hormonal Changes in First-Time Human Fathers in Relation to Paternal Investment Oxytocin levels rise across the gestational period in new fathers too, mirroring a pattern seen in mothers, though in fathers oxytocin levels were not linked to paternal involvement in the way researchers expected. Cortisol levels showed no difference between fathers and non-fathers. These findings suggest that the transition to parenthood involves hormonal preparation in both partners, though the mechanisms driving changes in the father are still largely unknown.
Conflict Built into the System
One reason pregnancy hormones are so complex is that the mother and fetus do not have perfectly aligned interests. From an evolutionary standpoint, the fetus benefits from extracting as many resources as possible, while the mother’s body benefits from preserving resources for her own survival and future pregnancies. This tension, sometimes called maternal-fetal conflict, is thought to have driven the evolution of placental hormone secretion itself.28PubMed. Maternal-fetal resource allocation: co-operation and conflict The placenta, which is genetically part of the fetus, secretes hormones like hPL that push the mother’s metabolism toward insulin resistance, freeing up glucose for fetal use. The mother’s pancreas compensates by producing more insulin. Gestational diabetes may represent a failure of this compensation, where the mother’s insulin production cannot keep pace with the placental hormones driving resistance. The condition can affect up to a quarter of pregnancies depending on the population studied and the diagnostic criteria used.