Preeclampsia is described, almost universally, as a disease of the mother. And there is admission that the causes may not be well understood. The patient is the mother. The mother’s blood pressures increases. The mother’s kidneys are stressed. The seizures, when they come as the preeclamsia becomes eclampsia, are the mother’s. The maternal mortality statistics are of the mother. The educational materials given to expecting couples in the obstetrician’s office are addressed, in tone and structure, to her.
The disease, however, is not the mother’s alone. A great deal of what determines whether a given pregnancy will become preeclamptic is contributed by the father’s genetics, by the father’s immunology, by the history of the couple before the pregnancy began, and in some cases by the conditions of the father’s own birth a generation earlier. The science on this has been accumulating for decades. Neither the clinical practice nor public understanding has caught up. As a result, fathers have been left out of a disease for which they are at least half responsible.
The evidence that preeclampsia has a substantial paternal component is not new or obscure. It is summarized in standard textbooks of obstetrics, but the implications have not been carried into routine clinical prenatal practice.
It has long been taught that first pregnancies are higher-risk for preeclampsia than subsequent pregnancies. The fuller story is that the risk is concentrated in the first pregnancy from a male partner. A woman with three healthy pregnancies with one man will have the elevated preeclampsia risk of a first pregnancy again with a new partner. The disease is responding not to whether she has been pregnant before, but to whether she has been pregnant before with this partner.
A woman who has had preeclampsia with one partner is at elevated, but not certain, risk of preeclampsia with a different partner. A woman who has had a healthy pregnancy with one partner can develop preeclampsia with a different partner. The partner-specific risk pattern is one of the clearest signals that the disease is responding to the couple, not to the woman in isolation.
This is the corollary that often surprises people. A man who has fathered a preeclamptic pregnancy with one partner is at elevated risk of fathering a preeclamptic pregnancy with a different partner. A man who was himself the product of a preeclamptic pregnancy is at elevated risk of fathering a preeclamptic pregnancy. The transgenerational inheritance of preeclampsia risk runs not only through the mother’s line, but also through the father’s line as well. The condition that complicated a man’s own birth is part of what he carries into his role as a father a generation later, transmitted through his genetics and through the placenta his contribution helps to build.
Couples who have been together longer, with regular exposure to one another’s biology, develop lower preeclampsia risk in their pregnancies. Couples who conceive shortly after meeting — and especially couples who conceive in the first few months of being together — have higher preeclampsia risk than couples who have been together for years.
The maternal immune system, with sustained exposure to a particular male partner’s biology in the months and years before pregnancy, develops a tolerance to his antigens. That tolerance is part of what allows the placenta — half of which is paternal tissue — to be accepted without provoking the inflammatory immune response that preeclampsia in part represents.
Pregnancies achieved with donor sperm or donor eggs show elevated preeclampsia risk. The mother’s immune system has not had the months or years of exposure to the donor’s antigens that it would have had with her partner. Surrogacy presents the most extreme version of immunologic novelty: a carrying mother whose immune system has no genetic relationship to either the egg or the sperm that produced the pregnancy. The preeclampsia risk in gestational surrogacy is elevated for the same reason.
Clinicians and couples involved in assisted reproduction need to know about the elevated risk, to monitor for it carefully, and to plan accordingly.
The structure of prenatal care, as it has evolved over the past several decades, has progressively narrowed the father’s role to the moment of conception and the moment of birth, with everything in between treated as the mother’s domain. The father shows up to the twelve-week ultrasound and to the twenty-week anatomy scan because the office permits him to. He is not, in any meaningful clinical sense, a patient of the practice. And when the pregnancy is complicated by a disease he has contributed half of, no one tells him so.
Bringing fathers back into the prenatal visit, into the discussion of preeclampsia and of every other complication of pregnancy, into the planning of the birth and into the early weeks of the newborn’s life, is not a courtesy to fathers. It is a recognition of what they bring to the family.
Ask your obstetrician about preeclampsia at your first prenatal visit. If the obstetrician seems surprised by the question or unprepared to include the father, you should know that some practices are better than others at including fathers. The point of the question is not to put the obstetrician on the spot. The point is to begin the pregnancy with the right people in the room.
Bringing the father back into the prenatal picture is, in part, a matter of accurate science. The biology of preeclampsia is the biology of an immunologic relationship between two contributing parties and the tissue they have built together. To describe it any other way is to describe it incompletely.