Morning sickness has a strong genetic component. A large twin study estimated that 73% of whether a woman experiences nausea and vomiting during pregnancy is determined by heritable factors. Genetics also influence how long symptoms last (about 51% heritable) and how severe they get (about 53% heritable). So if your mother or sister had rough pregnancies, your chances of a similar experience are meaningfully higher.
How Strong Is the Family Link?
The numbers here are striking. Women who had the most severe form of morning sickness, called hyperemesis gravidarum, were far more likely to have a sister who also suffered from it. In one study, sisters of affected women had 17 times the odds of developing hyperemesis gravidarum themselves compared to the general population.
The maternal connection is similarly clear. Among women hospitalized for severe pregnancy nausea, 33% reported that their own mother had experienced the same condition. Only 8% of women without severe symptoms said the same. That fourfold difference points to something being passed down, not just through shared environment or diet, but through DNA.
The Genes Behind It
Scientists have identified two genes that play a central role. The first, GDF15, produces a protein that acts on a receptor in the brainstem tied to nausea and appetite suppression. During pregnancy, the placenta floods the bloodstream with this protein. Women whose bodies aren’t accustomed to high levels of it before pregnancy appear to react more intensely, triggering worse nausea and vomiting.
The second gene, IGFBP7, sits on a different chromosome and is also involved in placental development and appetite regulation. A genome-wide study found that variants in both GDF15 and IGFBP7 reached the highest level of statistical significance for association with hyperemesis gravidarum, and the findings were confirmed in an independent group of patients. Interestingly, both genes serve dual purposes: they help maintain a healthy pregnancy while simultaneously raising the risk of nausea. That tradeoff may explain why these genes persist in the human population rather than being weeded out over time.
Why These Genes Survived Evolution
If morning sickness is so miserable, why hasn’t natural selection eliminated the genes that cause it? The leading theory is that nausea during early pregnancy actually protects the developing embryo. The idea, first proposed in the 1970s and supported by subsequent data, is that morning sickness drives women to avoid foods most likely to carry harmful microorganisms or natural toxins, particularly meats, strong-tasting vegetables, and certain beverages. Before refrigeration existed, these food aversions would have reduced the risk of infection or exposure to chemicals that could damage a developing fetus.
This “prophylactic” hypothesis fits with the timing of morning sickness. Symptoms typically peak during the first trimester, when embryonic organ development is most vulnerable to disruption. Women who carried gene variants producing stronger nausea responses may have had slightly better pregnancy outcomes over thousands of generations, keeping those variants common in the gene pool.
What Determines Your Severity
Your genetic variants set the stage, but the mechanism is more nuanced than simply inheriting a “morning sickness gene.” The key factor appears to be the gap between your body’s baseline exposure to the GDF15 protein before pregnancy and the surge the placenta produces once you conceive. Women who naturally produce lower levels of GDF15 before pregnancy experience a sharper spike when the placenta starts pumping it out, and that sudden change is what overwhelms the nausea receptors in the brain.
This explains a few patterns that have puzzled doctors. Women with certain blood disorders that chronically elevate GDF15 levels, like beta-thalassemia, rarely experience morning sickness. Their bodies are already desensitized to the protein before pregnancy begins, so the placental surge doesn’t register as strongly. On the flip side, women carrying genetic variants that keep pre-pregnancy GDF15 low are more vulnerable to severe symptoms.
The remaining 27% or so of risk that isn’t genetic likely involves factors like stress, diet, the number of fetuses, and individual hormone profiles. But genetics is by far the largest single contributor.
What This Means for Treatment
Understanding the GDF15 mechanism has opened a new avenue for prevention. Researchers are exploring whether exposing women to small amounts of the GDF15 protein before pregnancy could desensitize the brain’s nausea receptors, essentially training the body to tolerate the surge that comes with the placenta. Early-phase safety trials of a synthetic version of the protein (in non-pregnant volunteers) have been completed.
Another approach under investigation involves metformin, a widely used diabetes medication that happens to raise GDF15 levels. The idea would be to use it before conception in women known to be at high risk, gradually building tolerance. Researchers have also proposed engineered antibodies that could block the nausea signal during pregnancy without crossing into the placenta and affecting the fetus. None of these approaches are available as treatments yet, but they represent the first time scientists have had a clear molecular target for morning sickness prevention rather than just managing symptoms after they start.
If your mother or sister had severe morning sickness, your genetic risk is real and quantifiable. That information is worth sharing with your care team early in pregnancy so symptom management can begin before things escalate.