Although Attention-Deficit/Hyperactivity Disorder shows (ADHD) male predominance, females are significantly impaired and exhibit additional comorbid disorders during adolescence. However, no empirical work has examined the influence of cyclical fluctuating steroids on ADHD symptoms in women. The present study examined estradiol (E2), progesterone (P4), and testosterone (T) associations with ADHD symptoms across the menstrual cycle in regularlycycling young women (N=32), examining trait impulsivity as a moderator. Women completed a baseline measure of trait impulsivity, provided saliva samples each morning, and completed an ADHD symptom checklist every evening for 35 days. Results indicated decreased levels of E2 in the context of increased levels of either P4 or T was associated with higher ADHD symptoms on the following day, particularly for those with high trait impulsivity. Phase analyses suggested both an early follicular and early luteal, or post-ovulatory, increase in ADHD symptoms. Therefore, ADHD symptoms may change across the menstrual cycle in response to endogenous steroid changes.

Introduction

Attention-Deficit/Hyperactivity Disorder (ADHD) is a common and impairing childhood neurodevelopmental disorder (APA, 2013; Bernfort et al., 2008; Pelham et al., 2007, Polanczyk et al., 2007; Sayal et al. 2017; Thomas et al., 2015) that often persists into adolescence and adulthood with a prevalence of approximately 3% in adults (Faraone & Biederman, 2005; Fayyad et al., 2017; Kessler et al., 2006; Wilcutt, 2012). ADHD is a heterogeneous condition, currently conceptualized theoretically using multiple pathway models (Nigg et al., 2004; SonugaBarke, 2005) and most accurately described using two continuous symptom dimensions of inattention and hyperactivity-impulsivity (Haslam et al., 2006; Larsson et al., 2012; Marcus & Barry, 2011). Although ADHD is more frequently diagnosed in males, females with ADHD often become particularly impaired and exhibit comorbid disorders beginning during adolescence (Biederman et al., 1999; Hinshaw et al., 2012; Hosain, et al., 2012; Lahey et al. 1994; Quinn, 2005; Robison et al., 2008). The mechanisms of such sex differences remain unclear yet fundamental to understanding ADHD and sex differences in ADHD. Prior work suggests a role for organizational testosterone (T) in ADHD symptoms in both sexes (Wang et al., 2017), but particularly males (Martel, 2009; McFadden et al., 2005). Women and girls are under-studied and in particular, activational hormonal effects remain essentially unstudied in ADHD. Case studies have suggested that ADHD symptoms may worsen the week before menstruation (during declining estrogen and progesterone; Quinn, 2005) and improve during pregnancy (during elevated estrogen and progesterone (Nadeau & Quinn, 2002), but empirical work is lacking. Higher estradiol (E2) and progesterone (P4) have been generally linked to enhanced executive function (EF) and attention (e.g., Hatta & Nagaya, 2009), which appear to improve during cycle phases characterized by elevated E2 and P4 (Gogos, 2013; Howard et al., 1988; Jacobs & D’Esposito, 2011; Lord & Taylor, 1991; Rosenberg & Park, 2002; Segal, 2012; Vranic ́ & Hromatko, 2008; Solís-Ortiz & Corsi-Cabrera, 2008; Solis-Ortiz et al., 2004). Further, verbal fluency, verbal learning and memory appear to improve with administration of T in women (Davison et al., 2011; Drake et al., 2000), whereas response inhibition performance decreases (Bjork et al., 2001). Given that weak EF is a prominent correlate and possible marker of ADHD, this prior work suggests a potential role for cycling reproductive steroids in daily ADHD symptom expression.