Medication, which Americans favor over other forms of therapy, poses risks to a developing fetus, but so does having a depressed mother
There's no denying that we pass diseases down from one generation to the next, thanks to our genes and/or the climate in which we raise our children. The classic example is overweight parents with overweight kids. They have inherited a gene linked to obesity or picked up poor eating habits, or both. But this phenomenon doesn't just apply to physical diseases and disorders. Oh no. We also pass our mental health issues down to our kids, from little personality quirks to more serious problems, like worry, anxiety, obsessions, compulsions, and depression.
Depression is a prime example of a disorder that runs through both genes and the environment. When a woman is pregnant, the chemical environment in her body and brain has an effect on her fetus' development. And when this "climate" is off, as in the case of depression, it seems to lead to a specific set of psychological and physiological risks to the child -- from premature birth to emotional and social problems -- that are distinct from those associated with mental health issues in other periods of maternal life. And new research is asking whether, when it comes to the child's health, it's better to treat depression during pregnancy or just leave it alone.
It's actually better for the baby if his or her mother's depression stays consistent between pregnancy and birth than if it lifts.
Antidepressants, which Americans are increasingly favoring over other forms of therapy, come with a significant set of risks to the developing fetus, which are expressed in both the brain and behavior of the offspring. A recent study found that one of the most widely used classes of antidepressants, selective serotonin uptake inhibitors (SSRIs), given to rats in the perinatal period -- just before and after birth -- had a significant effect on brain development. This "critical period" in rodents is thought to correspond to the third trimester in humans.
The fetal and neonatal rats exposed to SSRIs showed altered electrical activity in the brain, and reductions in a major serotonin circuit, the raphe system. They also had deformations in the corpus callosum, the bundle of fibers that allows the transfer of information between the two hemispheres of the brain: specifically, there were deficiencies in the cells' insulation, the myelin sheath, which swathes nerve fibers to speed communication. Physiological changes are usually expressed in behavioral changes, and this was true here, too: The animals given SSRIs showed a reluctance to explore new environments and an exaggerated fear response to a novel sound. These alterations in rodent behavior are thought, significantly, to mirror autism in humans.
This SSRI-autism connection is not new, and it's not distinct to rodents. In fact, a study earlier in the year suggested that using antidepressants during pregnancy is linked to a greater risk of autism in human children. The mothers of children on the autism spectrum were three times as likely to have been on antidepressants during the first trimester of pregnancy. While this doesn't nail down cause-and-effect, the researchers controlled for enough variables -- like maternal age and education, sex of the child, birth weight, and how complicated the birth -- that the link seems likely, particularly in light of the new study.