The placenta produces at least seven major hormones that sustain pregnancy, protect the fetus, and reshape the mother’s metabolism from the first weeks after conception through delivery. Some of these hormones are familiar from pregnancy tests, while others work behind the scenes to redirect nutrients, suppress contractions, and even set the timing of labor.
Human Chorionic Gonadotropin (hCG)
hCG is the hormone detected by pregnancy tests, and it’s the first major signal the placenta sends. Specialized placental cells called trophoblasts begin releasing hCG about one day after the embryo implants in the uterine wall, roughly eight days after ovulation. Its primary job is to rescue a small ovarian structure called the corpus luteum, which would otherwise break down at the end of a normal menstrual cycle. By keeping the corpus luteum alive, hCG ensures it continues pumping out progesterone, the hormone that holds early pregnancy in place.
hCG levels rise rapidly in the first trimester, peaking around week 10 with values that can reach nearly 300,000 mIU/mL. After that peak, levels gradually decline for the rest of pregnancy. This steep early rise is why pregnancy symptoms like nausea tend to be strongest in the first trimester. hCG is also one of the blood markers used in prenatal screening for chromosomal conditions such as Down syndrome.
Progesterone
Progesterone is arguably the single most important hormone for maintaining a pregnancy, and the placenta becomes its primary source surprisingly early. Between weeks 7 and 9, a transition called the luteal-placental shift occurs: the placenta takes over progesterone production from the corpus luteum. By the time a pregnancy reaches full term, the placenta is producing roughly 250 milligrams of progesterone per day, with blood levels reaching 100 to 200 ng/mL.
Progesterone keeps the uterus quiet. It prevents premature contractions by dampening the electrical activity of uterine muscle cells, essentially raising the threshold those cells need to fire. It does this partly by increasing the activity of potassium channels that keep muscle cells relaxed and by reducing levels of proteins involved in muscle contraction. Without adequate progesterone, the uterus would begin contracting too early.
Progesterone also plays an immune role. The fetus carries genetic material from both parents, which means the mother’s immune system could theoretically recognize it as foreign tissue. Progesterone shifts the immune response toward a more tolerant profile, suppressing the type of immune activity that would attack the placenta and fetus. One notable feature of placental progesterone production: it’s remarkably stable. Unlike estrogen, which depends on precursors from the fetus, progesterone output continues regardless of fetal health or available precursor supply.
Estrogens
The placenta produces three forms of estrogen: estradiol, estrone, and estriol. What makes placental estrogen production unusual is that the placenta can’t do it alone. It lacks certain enzymes needed to build estrogen from scratch, so it depends on raw materials supplied by the fetal adrenal glands and liver. The fetus produces about 90% of a key precursor called 16α-hydroxy DHEA-S, which the placenta then converts into estriol. This partnership between the fetal organs and the placenta is sometimes called the fetal-placental unit.
Estrogens increase blood flow to the uterus, stimulate breast tissue development, and help prepare the body for labor and breastfeeding. Because estriol production depends so heavily on fetal contributions, estriol levels in the mother’s blood were historically used as a marker of fetal well-being. Estriol is still measured as part of some prenatal screening panels.
Human Placental Lactogen (hPL)
Human placental lactogen reshapes the mother’s metabolism to prioritize the fetus. Its main effect resembles that of growth hormone: it makes the mother’s tissues more resistant to insulin. This insulin resistance isn’t a malfunction. It’s a deliberate strategy that limits how much glucose the mother’s cells absorb, keeping more glucose circulating in the bloodstream where it can cross the placenta and fuel fetal growth.
To compensate, hPL triggers the breakdown of stored fat into free fatty acids, giving the mother an alternative energy source. This is why fasting pregnant women experience what’s sometimes called “accelerated starvation,” where blood sugar drops more quickly than it would outside of pregnancy. As blood sugar falls, hPL levels rise to accelerate fat breakdown and spare glucose for the fetus. The system works like a seesaw: when maternal glucose dips, hPL pushes harder on fat stores to keep the mother fueled while protecting fetal energy supply. In some women, the insulin resistance driven by hPL and other placental hormones can tip into gestational diabetes.
Placental Growth Hormone
Distinct from the growth hormone produced by the pituitary gland, placental growth hormone (PGH) is unique to pregnancy. It gradually replaces pituitary growth hormone in the mother’s circulation and works primarily by raising levels of a growth-promoting protein called IGF-1. Higher IGF-1 stimulates the mother’s body to produce more glucose, break down more fat, and build new tissue, all of which increases the pool of nutrients available to the fetus.
PGH responds directly to the mother’s blood sugar and insulin levels. When glucose is low, PGH output rises to mobilize more nutrients. Studies have found a positive correlation between PGH levels and birth weight: higher PGH generally means a larger baby, while reduced PGH expression is associated with restricted fetal growth. Beyond metabolism, PGH also promotes the invasion and development of placental tissue itself, helping the placenta establish a strong connection with the uterine blood supply.
Corticotropin-Releasing Hormone (CRH)
Outside of pregnancy, CRH is primarily a brain hormone involved in the stress response. The placenta produces its own version, and levels rise exponentially throughout pregnancy. Researchers have proposed that placental CRH acts as a kind of biological clock that helps determine when labor begins.
In a landmark 1995 study, women who delivered preterm had higher CRH levels earlier in pregnancy, while women who delivered late had lower levels. These differences were detectable as early as 16 to 18 weeks. The theory is that once placental CRH rises high enough to overwhelm the proteins that normally bind and inactivate it in the bloodstream, the free CRH helps trigger the cascade that initiates labor. CRH does this partly by boosting estriol production and activating signaling pathways that make the uterine muscle more contractile. In most pregnancies, this clock runs on schedule. In a subset of women, early CRH elevation may contribute to preterm birth.
Relaxin
Relaxin is a small hormone in the insulin-like growth factor family that influences connective tissue throughout the body. During pregnancy, it’s associated with remodeling of collagen, the protein that gives ligaments and joints their structure. The pelvic ligaments begin to loosen around weeks 10 to 12, a physical change that helps accommodate the growing uterus and eventually allows the pelvis to widen during delivery.
Relaxin has traditionally been credited with this loosening, though the relationship is more complex than once thought. Some studies have found that higher relaxin levels don’t consistently predict greater pelvic mobility or joint laxity in individual women. The hormone likely works in concert with progesterone and estrogen rather than acting as a sole driver. Still, the broader effect on connective tissue is real, which is why many pregnant women notice increased flexibility and joint instability that can persist for weeks after delivery.
Inhibin A
Inhibin A is a protein hormone produced by the placenta that plays a role in regulating reproductive signaling. Its most practical relevance for most people is in prenatal screening. Inhibin A is one of the four blood markers used in the “quad screen,” a second-trimester test that estimates the risk of Down syndrome and other chromosomal conditions. Elevated inhibin A levels, combined with the other markers and factors like maternal age, help identify pregnancies that may benefit from further diagnostic testing.
How These Hormones Work Together
No single placental hormone works in isolation. hCG keeps progesterone flowing in early pregnancy, then the placenta takes over progesterone production directly. Progesterone keeps the uterus calm while estrogen prepares it for eventual labor. hPL and placental growth hormone both push the mother’s metabolism toward insulin resistance, with overlapping but distinct mechanisms, to funnel nutrients toward the fetus. CRH quietly accumulates in the background, eventually helping to override progesterone’s calming influence and initiate contractions.
The placenta functions as a temporary but powerful endocrine organ, one that coordinates the biology of two separate people for roughly nine months and then, after delivery, is no longer needed. The sudden loss of all these hormones at birth is one reason the postpartum period involves such dramatic physical and emotional shifts.