The placenta is not made from sperm, but the claim contains a grain of biological truth that makes it stubbornly persistent on social media. The placenta grows from the same fertilized cell that becomes the baby, so it carries DNA from both parents in roughly equal measure. What gives the myth its staying power is a genuinely surprising finding: the father’s genes are disproportionately active in placental tissue, and sperm can carry epigenetic marks that shape how the placenta develops and functions. The reality is more interesting than the headline version.
How the Placenta Actually Forms
After a sperm fertilizes an egg, the resulting single cell divides repeatedly over the next several days. By about five days after fertilization, this cluster of cells has organized itself into a hollow ball called a blastocyst. At this stage, the very first fork in the road of human development occurs: some cells become the inner cell mass, which will eventually form the baby, and the outer ring of cells becomes the trophectoderm, which will become the placenta and its supporting membranes.1PubMed. Cdx2 is required for correct cell fate specification and differentiation of trophectoderm in the mouse blastocyst Both lineages descend from the same fertilized egg, so both carry a full set of chromosomes, half from the mother and half from the father.
This means the placenta is no more “made from sperm” than the baby is. Both are products of a union between egg and sperm. Research on pregnancies where embryos fail to develop normally but trophoblast tissue still grows has confirmed that even in those cases, the placental tissue contains DNA from both parents.2PubMed. Trophoblast from anembryonic pregnancy has both a maternal and a paternal contribution to its genome At the surface level of raw genetics, the placenta is a 50/50 proposition.
Why Dad’s Genes Are Disproportionately Active in the Placenta
Here is where the simple answer gets complicated. Your cells carry two copies of most genes, one inherited from each parent, and in most tissues both copies are switched on and contribute equally. But a subset of genes behave differently: only one copy is active, and which copy that is depends on whether it came from mom or dad. This phenomenon is called genomic imprinting, and it is especially pronounced in the placenta.
A study that systematically catalogued imprinted genes found that paternally expressed genes predominate in placental tissue. Among a core group of 15 ancient imprinted genes, 10 were paternally expressed. An additional 78 candidate imprinted genes also showed a paternal bias, and these genes displayed parent-of-origin expression bias in the placenta but not in the fetus itself.3PubMed Central. Paternally expressed genes predominate in the placenta So while both parents contribute equal amounts of DNA to the placenta, the father’s copies of certain genes are doing more of the talking.
There is even a layer of imprinting that affects entire chromosomes. In the placenta and other tissues derived from the trophectoderm, it is preferentially the father’s X chromosome that gets silenced in female embryos, while the mother’s X stays active. In the embryo proper, X inactivation is random.4Development. Preferential paternal X inactivation in extraembryonic tissues of early mouse embryos This selective silencing of the paternal X in placental tissue is yet another way that gene expression in the placenta differs from the rest of the developing organism.
The net effect is that the placenta is a place where paternal genetic influence is amplified relative to what you’d expect from looking at DNA sequences alone. This is probably the kernel of truth that gets inflated into “the placenta is made from sperm.”
What Happens When Only One Parent’s Genome Shows Up
Some of the most striking evidence for the father’s role in placental growth comes from pregnancies that go wrong in very specific ways. A complete hydatidiform mole is a pregnancy in which the entire genome comes from the father, with no maternal genetic contribution. Instead of forming a baby, the tissue proliferates into a mass of abnormal placental villi that resemble a cluster of grapes. There is rampant trophoblast growth but no functioning embryo. The overrepresentation of the paternal genome leads to global disruption of imprinted gene expression, driving the uncontrolled placental tissue growth that defines the condition.5PubMed. Hydatidiform Moles: Genetic Basis and Precision Diagnosis
The mirror image is equally telling. Embryos that carry only maternal chromosomes and no paternal contribution, called gynogenetic embryos, die at or soon after implantation.6PubMed. The development of XO gynogenetic mouse embryos They fail to build a functional placenta. This pair of outcomes suggests a kind of lopsided partnership: two copies of dad’s genome and none of mom’s produces excessive placental growth but no baby, while two copies of mom’s genome and none of dad’s produces a stunted placenta that cannot sustain a pregnancy at all. Normal development requires both contributions, but the paternal genome appears to be the stronger driver of placental tissue expansion specifically.
The Evolutionary Tug-of-War Behind Imprinting
Why would evolution set things up so that dad’s genes push for more placental growth while mom’s genes act as a brake? The leading explanation is a theory of evolutionary conflict between parental interests. In species where a mother may carry offspring fathered by different males over her lifetime, the father’s genes “want” the current pregnancy to extract as many resources from the mother as possible, since his other offspring are likely being carried by other females. The mother’s genes, on the other hand, “want” to spread resources evenly across all her pregnancies, present and future.7PubMed Central. Placental imprinting: Emerging mechanisms and functions
This predicts exactly the pattern researchers observe: growth-enhancing genes in the placenta tend to be paternally expressed, and growth-suppressing genes tend to be maternally expressed.8Population Ecology. Conflict theory of genomic imprinting in mammals Studies of human pregnancies have found that paternally expressed imprinted genes in the placenta are associated with promoting fetal growth, while maternally expressed imprinted genes are linked to growth restraint, consistent with what the theory predicts.9PubMed Central. Associations between imprinted gene expression in the placenta, human fetal growth and preeclampsia
This tug-of-war plays out every day inside a pregnant person’s body. The placenta remodels the mother’s uterine blood vessels, replacing endothelial and muscle tissue to widen the arteries and increase blood flow to the fetus. When this remodeling fails, it can contribute to preeclampsia, a dangerous condition involving high blood pressure.10PubMed Central. Uterine spiral artery remodeling involves endothelial apoptosis induced by extravillous trophoblasts through Fas/FasL interactions The trophoblast cells doing this remodeling are aggressive invaders by design, driven in part by paternally biased gene expression. The mother’s body tolerates this invasion partly through specialized immune signaling at the placental interface.
How Sperm Epigenetics Can Shape the Placenta
Beyond the DNA sequence itself, sperm carry a set of chemical marks on their DNA, primarily methyl groups attached to specific locations, that can influence which genes get turned on or off after fertilization. These epigenetic marks are one mechanism through which a father’s environment and health can leave a fingerprint on placental development, and this is the part of the story that most closely approaches “sperm affecting the placenta.”
A 2024 study found that men whose partners developed early-onset preeclampsia had disrupted methylation patterns in their sperm at imprinted gene locations, and that the placentae from those pregnancies showed impaired expression of the same imprinted genes.11PubMed. Methylation aberrations in partner spermatozoa and impaired expression of imprinted genes in the placentae of early-onset preeclampsia The researchers highlighted this as evidence for a direct paternal contribution to the condition, mediated through sperm epigenetics rather than through the DNA sequence itself.
Paternal age adds another dimension. A study comparing sperm and placental methylation patterns found that DNA methylation changes associated with advanced paternal age in spermatozoa overlapped with methylation changes in placental tissue. Several of the affected genes were also susceptibility genes for autism spectrum disorder, based on a widely used gene database, suggesting that placental epigenetic marks may reflect aging-related changes originating in sperm even in healthy pregnancies.12PubMed Central. Advanced Paternal Age Impacts Common Loci in the Sperm and Placenta DNA Methylomes
Animal studies have taken this a step further by looking at environmental exposures. In a mouse model, paternal exposure to a developmental toxicant altered methylation at specific gene locations in the father’s sperm, and those same methylation changes appeared in the placentae of his offspring, persisting even to a later generation.13Biology of Reproduction. Paternal developmental toxicant exposure is associated with epigenetic modulation of sperm and placental Pgr and Igf2 in a mouse model This is still a mouse finding and should be interpreted cautiously, but it illustrates a plausible pathway by which a father’s exposures could influence placental function through epigenetic inheritance.
Sperm also deliver small amounts of RNA into the egg at fertilization. Compared to the large stockpile of RNA the egg already contains (roughly a thousand times more), the sperm’s contribution is tiny. But pooled human sperm contain thousands of different messenger RNA sequences and dozens of small regulatory RNA molecules, some of which may specifically affect genes active during early embryo development.14Theriogenology / Elsevier. A possible role for sperm RNA in early embryo development Whether these sperm-delivered RNAs meaningfully shape the trophectoderm lineage that becomes the placenta is still an open question, but the delivery mechanism exists.
Fertility Treatments and the Placenta
Given how sensitive placental imprinting is, a natural question is whether fertility procedures that bypass normal sperm selection and fertilization alter placental development. The evidence so far is largely reassuring. A study comparing pregnancies conceived through in vitro fertilization, intracytoplasmic sperm injection (where a single sperm is injected directly into the egg), and natural conception found no significant differences in DNA methylation at a key imprinted gene region in the placenta.15Theriogenology / Elsevier. DNA methylation at H19/IGF2 ICR1 in the placenta of pregnancies conceived by in vitro fertilization and intracytoplasmic sperm injection
One study did find that pregnancies conceived using sperm surgically retrieved from the testicle had placentas that were about 15% larger at 11 weeks of gestation compared to pregnancies conceived with ejaculated sperm. However, embryonic growth milestones did not differ between the groups.16PubMed Central. The impact of the origin of surgical sperm retrieval on placental and embryonic development: The Rotterdam Periconception cohort The clinical significance of this early placental volume difference is unclear, but it suggests that the maturity or origin of the sperm may subtly affect early placental growth without necessarily changing embryonic development.
How the Placenta Hides From the Mother’s Immune System
Because the placenta carries paternal DNA, it is immunologically foreign to the mother, which raises an obvious puzzle: why doesn’t the mother’s immune system attack it? Part of the answer involves a molecule called HLA-G, produced by the invasive trophoblast cells at the maternal-fetal interface. HLA-G interacts with receptors on multiple types of maternal immune cells, including T cells, natural killer cells, and macrophages, essentially telling them to stand down. It is widely regarded as a key protective factor for successful pregnancies.17PubMed Central. HLA-G: An Important Mediator of Maternal-Fetal Immune-Tolerance
In equine pregnancies, researchers have shown that both maternally and paternally inherited immune-related molecules are expressed together by trophoblast cells, rather than only one parent’s version being displayed.18PubMed. Paternal and maternal major histocompatibility complex class I antigens are expressed co-dominantly by equine trophoblast This co-expression means the placenta is not hiding the father’s identity so much as managing the immune response to it. The system is finely tuned: enough immune tolerance to protect the pregnancy, but enough immune surveillance to prevent abnormal cell growth.
Ancient Viruses Built Part of the Placenta
One of the stranger chapters in placental biology has nothing to do with sperm or eggs as we usually think of them. Key genes responsible for the physical structure of the placenta were originally viral genes, captured from retroviruses that infected our distant ancestors. These genes, called syncytins, produce proteins that fuse neighboring cells into a continuous barrier layer called the syncytiotrophoblast, which is the part of the placenta directly bathed in maternal blood.
Humans have two syncytin genes, mice have a different pair, and rabbits have yet another, all independently acquired from different retroviral infections at different points in evolutionary history. In mice, knocking out either of the two syncytin genes disrupts the formation of the corresponding placental barrier layer, confirming that these repurposed viral genes are genuinely essential for building a functional placenta.19PubMed Central. A pair of co-opted retroviral envelope syncytin genes is required for formation of the two-layered murine placental syncytiotrophoblast The convergent evolution here is remarkable: different mammalian lineages independently recruited different viral genes to solve the same problem of creating a placental exchange surface. These syncytin genes sit in the genome like any other gene, inherited from both parents through normal chromosomal transmission, and have nothing to do with the “sperm makes the placenta” narrative. But they do illustrate that the placenta’s origins are far stranger and more patchwork than most people realize.