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Prenatal Paternal Selective Serotonin Reuptake Inhibitors Use and Risk of ADHD in Offspring

OBJECTIVES:

It has been shown that maternal prenatal exposure to selective serotonin reuptake inhibitors (SSRIs) may be a risk factor for attention-deficit/hyperactivity disorder (ADHD) in offspring. Our goal was to examine whether paternal SSRI use before conception increases the risk of ADHD in offspring.


METHODS:

On the basis of Danish national registers, we conducted a cohort study of 781 470 singletons born between 1996 and 2008 with follow-up throughout 2013. The children whose fathers used SSRIs during the last 3 months before conception were identified as the exposed. Cox regression was used to estimate the hazard ratio (HR) of ADHD.


RESULTS:

A total of 7216 children (0.92%) were born to fathers who had used SSRIs during the last 3 months before conception. There were 12 520 children diagnosed with ADHD. Compared with unexposed children, the exposed had a 26% increased risk of ADHD (HR = 1.26, 95% confidence interval [CI]: 1.06–1.51) after adjusting for potential confounders. When extending the exposure window to 1 year before conception, paternal use of SSRIs only during the period of 12 to 3 months before conception was associated with the HR of 1.35 (95% CI: 1.10–1.66), whereas paternal use of SSRIs only during the last 3 months before conception was associated with a similarly increased risk of ADHD (adjusted HR = 1.31, 95% CI: 0.95–1.82).


CONCLUSIONS:

The mildly increased risk of ADHD in offspring associated with paternal SSRI use before conception could probably be due to the underlying indications related to SSRI use.


RE: Prenatal Paternal SSRI Use effects ADHD risk

January 28 2018

Stephanie A.M. Satchell

MOREHOUSE SCHOOL OF MEDICINE

I have read the recent article entitled “Prenatal Paternal Selective Serotonin Reuptake Inhibitors Use and Risk of ADHD in Offspring” by Fen Yang et al published in January 2018 Pediatrics. I want to congratulate the authors on a successful research article. The topic was intriguing and innovative. The methods and research was very well thought out and executed. In addition to congratulations, I would like to offer some additional contributions.The authors briefly mention that SSRIs induce semen quality impairment and abnormal DNA fragmentation as background leading up to the hypothesis of SSRIs effecting ADHD risk in offspring. Nonetheless, they conclude that the observed increased risk of ADHD associated with paternal SSRI use before conception could apparently be a result of confounding by paternal psychopathology. I would like to offer additional recent research that may add to this conclusion. In a study from March 2017 in Birth Defects Research, citalopram induced testicular damage in male rats accompanied by oxidative stress as seen by decreased glutathione signaled [1]. Such oxidative stress can enhance the amounts of mutations already in DNA with specific mutations related to ADHD risk. In a more recent article from January 2018 in Psychiatry Clinical Neuroscience, copy number variants are highlighted to be associated with extraordinarily high levels of autism, schizophrenia, intellectual disability or ADHD [2]. With these additional articles in mind, it would be interesting to further delve into the genetics and inheritance of ADHD and the possible additive risks that SSRIs may pose.Specifically, it would be interesting to look at ADHD inheritance as similar to that involving genetic anticipation due to certain mutated expansions during gametogenesis, more common in paternal transmission. Investigations of specific gene locations involved in ADHD are of course underway, though different studies have already highlighted possible connections with dopamine transporters [3]. As concluded in this article, paternal psychopathology may very well be a leading factor in the risk of ADHD in offspring already. However, I believe it is still important to consider SSRIs adding to mutation expansion either through oxidative stress or direct abnormal morphology; thus, increasing chances of ADHD inheritance via genetic anticipation or worsening phenotypic expression.As previously stated, this article was one of the firsts to explore prenatal paternal SSRI exposure and ADHD risk. It was innovative, well implemented, and highlighted valid conclusions. However, I believe this study leads the way to further genetic investigation for ADHD etiology and does not yet rule out paternal SSRI use contributions to ADHD risk in offspring.


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