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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive Sept 12, 2014

For ADHD, the increased risk associated with prenatal antidepressant exposure remained
significant, although reduced, even after adjusting for the severity of maternal depression.

 






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No link between antidepressants and autism risk

Previous studies that suggest an increase in autism among children of women on antidepressants, may in fact reflect the statistical risk to children of mothers with severe depression.

While a diagnosis of autism spectrum disorder is more common in the children of mothers prescribed antidepressants during pregnancy than in those with no prenatal exposure – the severity of the mother's depression was what accounted for that increased risk making the increase no longer statistically significant.

However, an increased risk for attention-deficit hyperactivity disorder (ADHD), persisted even after controlling for factors relating to a mother's mental health.

The reports is published in Molecular Psychiatry, by investigators from Massachusetts General Hospital (MGH).


"We know that untreated depression can pose serious health risks to both a mother and child, so it's important that women being treated with antidepressants who become pregnant, or who are thinking about becoming pregnant, know that these medications will not increase their child's risk of autism."

Roy Perlis, MD, MSc, MGH Department of Psychiatry, senior author of the report.


While genetic factors are known to play a substantial role in autism, exactly how that risk may be exacerbated by environmental factors is not well understood. Some animal studies and investigations based on health records suggest an increased risk with prenatal antidepressant exposure. However, discontinuing antidepressant treatment significantly increases a risk of relapse – including an increased risk in postpartum depression. Therefore, the current study aimed to clarify whether or not any increase in autism risk is actually attribuatal to medication.

The research team analyzed electronic health records for children born at MGH, Brigham and Women's Hospital, or Newton Wellesley Hospital – all belonging to Partners HealthCare System – with a diagnostic code for pervasive developmental disorder (which includes autism) entered at least once between 1997 and 2010. Almost 1,400 such children were matched with more than 4,000 children with no autism diagnoses, all born the same years and matched for similar demographics.

This information was paired with that of mothers with a diagnosis for major depression or other mental illness, and receiving treatment including prescriptions for antidepressants and other psychotropic drugs. A similar analysis was done for almost 2,250 children with an ADHD diagnosis, compared to more than 5,600 with no ADHD diagnoses.

In the autism-focused comparison, after adjusting for indications of more severe maternal depression, the strength of the comparison was reduced to an insignificant level. Moreover, antidepressants with action stronger in the serotonin pathway — suspected of contributing to a possible autism risk — did not reflect an autism increase.


Children of mothers with severe morning sickness, who took a serotonin-targeting non-antidepressant drug as treatment, had no increased autism incidence either.

Prescriptions for antipsychotic drugs sometimes used to treat severe, treatment-resistant depression, as well as psychotic disorders, did appear to increase the risk for autism.

But for ADHD, the increased risk associated with prenatal antidepressant exposure remained significant, although reduced, even after adjustment for the severity of maternal depression.


"There are a range of options – medication and non-medication – for treating depression and anxiety in pregnancy. But if antidepressants are needed, I hope parents can feel reassured about their safety." adds Dr. Perlis.

Abstract
Prenatal antidepressant exposure is associated with risk for attention-deficit hyperactivity disorder but not autism spectrum disorder in a large health system

Previous studies suggested that risk for Autism Spectrum Disorder (ASD) may be increased in children exposed to antidepressants during the prenatal period. The disease specificity of this risk has not been addressed and the possibility of confounding has not been excluded. Children with ASD or attention-deficit hyperactivity disorder (ADHD) delivered in a large New England health-care system were identified from electronic health records (EHR), and each diagnostic group was matched 1:3 with children without ASD or ADHD. All children were linked with maternal health data using birth certificates and EHRs to determine prenatal medication exposures. Multiple logistic regression was used to examine association between prenatal antidepressant exposures and ASD or ADHD risk. A total of 1377 children diagnosed with ASD and 2243 with ADHD were matched with healthy controls. In models adjusted for sociodemographic features, antidepressant exposure prior to and during pregnancy was associated with ASD risk, but risk associated with exposure during pregnancy was no longer significant after controlling for maternal major depression (odds ratio (OR) 1.10 (0.70–1.70)). Conversely, antidepressant exposure during but not prior to pregnancy was associated with ADHD risk, even after adjustment for maternal depression (OR 1.81 (1.22–2.70)). These results suggest that the risk of autism observed with prenatal antidepressant exposure is likely confounded by severity of maternal illness, but further indicate that such exposure may still be associated with ADHD risk. This risk, modest in absolute terms, may still be a result of residual confounding and must be balanced against the substantial consequences of untreated maternal depression.

Caitlin Clements of the MGH Department of Psychiatry is lead author of the Molecular Psychiatry paper. Additional coauthors are Sarah Blumenthal, Hannah Rosenfield, Maurizio Fava, MD, Alysa Doyle, PhD, and Jordan Smoller, MD, ScD, MGH Psychiatry; Victor Castro , MD, and Shawn Murphy, MD, PhD, Partners Research Computing; Anjali Kaimal, MD, MAS, MGH Obstetrics and Gynecology; Elise Robinson, PhD, MGH Center for Human Genetic Research; Jane Erb, MD, and Isaac Kohane, MD, Brigham and Women's Hospital, and Susanne Churchill, PhD, Partners Information Systems. Support for the study includes National Institute of Mental Health grant R01MH086026 and support from the Stanley Center for Psychiatric Research.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $785 million and major research centers in HIV/AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

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