Having a Baby Makes Mom's Body Turn on Itself

The act of giving birth apparently raises the chance that a woman's body will attack itself with autoimmune diseases, a new study finds.

Scientists believe that cells from fetuses may flood into their mothers' blood and set off these disorders, but they caution this remains only speculation.

These findings might lead to new avenues of treatment for these disorders, researchers added.

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Autoimmune diseases such as lupus , rheumatoid arthritis and multiple sclerosis occur when a person's own immune system attacks his or her body. These disorders are more common among women, especially those of reproductive age lupus is nine times more likely to afflict women than men, rheumatoid arthritis four times and multiple sclerosis three times.

The question of whether pregnancy might help trigger these diseases has been debated for years. To shed light on the controversy, investigators analyzed medical records of more than 1 million women in Denmark born between 1962 and 1992. Of these, 43.4 percent had not been pregnant, 44.3 percent had their first pregnancy delivered conventionally, 7.6 percent had their first pregnancy delivered via cesarean section, and 4.1 percent had abortions. (The numbers do not quite add up because the women who had abortions did not all say whether they had other pregnancies.)

Of the approximately 1 million investigated, 25,570 developed autoimmune diseases. The researchers found that in the first year after conventional deliveries or cesarean sections, women had a 15 or 30 percent greater risk, respectively, of contracting such disorders. Surprisingly, this risk appeared 30 percent lower in the first year following abortion.

"These findings should apply to any group of women," said researcher Keelin O'Donoghue, a clinician scientist at University College Cork in Ireland.

The scientists knew from previous work in this field that cells from fetuses normally begin circulating in their mothers' blood very early in pregnancy and can be found in the bone marrow and other tissues of these women for decades afterward. They speculated that in attacking these foreign cells, the body inadvertently attacks itself as well. The act of giving birth can lead blood from the fetus to mingle with that of the mother, especially in the case of cesarean sections, where more blood crosses the placenta into the woman.

As to the unexpected finding of a lowered risk of autoimmune disease after abortion, the researchers conjectured that early loss of a fetus may allow more stem or similarly potent cells to enter the blood of these women, cell types more likely to prove beneficial than ones from later in fetal development. Previous lab work supports this notion, O'Donoghue noted.

There are a number of potential confounding factors this work faces. For instance, the effect the researchers observe might be due to how women normally get all kinds of medical tests when pregnant; if this is the case, this research could just be exposing autoimmune diseases that went undiagnosed beforehand. To account for such factors, comparing different groups of women who received differing levels of care during pregnancy could reveal the answer. We also need to consider the effect of further pregnancies on the risk of autoimmune disease over time," O'Donoghue said.

Understanding why autoimmune disease might develop after pregnancy may be of use to those planning or designing treatments for those various disorders.

"If the 'missing links' are the fetal cells persisting in the mother, then while fetal cell traffic cannot be prevented, it can be manipulated," O'Donoghue said. "This must be balanced against the proposed benefits of fetal cells for long-term maternal health."

Future research can look at this group of women over longer spans of time. "Longer follow-up may reveal more information about the impact of pregnancy," O'Donoghue said.

"Finally, we would like to explore further the impact of miscarriage," O'Donoghue added. "Many unanswered questions remain."

The scientists detailed their findings online May 18 in the journal PLoS ONE.

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