Pregnancy can delay the onset of multiple sclerosis (MS) by more than three years, according to an international study led by Victorian researchers.
Dr Ai-Lan Nguyen and Dr Vilija Jokubaitis from the Monash University Department of Neuroscience, analysed outcomes for more than 2557 women attending four MS clinics in two countries (Czech Republic, and Australia), who were enrolled in the MSBase database.
They found that women who have been pregnant had their first ‘clinically isolated syndrome’ neurological symptoms on average 3.3 years later compared to women who had never been pregnant.
A similar delay in CIS onset was also observed in women who had carried a baby to term – with onset delayed on average by 3.4 years.
However, no ‘dose effect’ for number of pregnancies or births was observed.
Dr Jokubaitis and co-authors say the findings add to previous Australian research showing a protective effect of pregnancy against demyelinating events, presumably via increased immune tolerance afforded by pregnancy.
“At present, we don’t know exactly how pregnancy slows the development of MS, but we believe that it has to do with alterations made to a woman’s DNA. We are now seeking funding opportunities to explore this exciting possibility,” she said.
An accompanying commentary article published in JAMA Neurology said the findings provided further evidence of reproductive factors, including sex steroid hormone production and pregnancy, altering the disease course in MS.
Previous studies have shown that pregnancy suppresses relapse activity, with the second and third trimesters having a more potent effect than the first trimester, noted Dr Jennifer Graves, of the Department of Neurosciences, University of California.
“The predominant oestrogen of pregnancy, oestriol, may be associated with relapse suppression, but a number of other biological changes in pregnancy could also mediate or play a role in this outcome.
“Other hormonal changes in pregnancy include high levels of progesterone, which has the capacity to modulate immune function in ways that fosters tolerance of the fetus, underpins changes in the expression of a number of immunologically important genes, and precipitates a general shift from a helper T cell 1 (TH1) to helper T cell 2 (TH2) phenotype,”
It is difficult to completely rule out reverse causation with pregnancy and MS, but the Australian study investigators tried to mitigate this issue by using age at onset (not risk) of MSas the primary outcome measure and to treat pregnancy as a time-dependent variable, the commentary noted.
“Just as pregnancy may prevent subsequent relapses in a woman’s MS course, it may forestall the first relapse. Understanding the precise biological mechanisms behind the suppression of relapses in pregnancy may elucidate pathways that are critical to understanding MS pathogenesis,” it concluded.