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Preclinical studies have demonstrated that conditioned fear extinction is impaired in females with low endogenous levels of the sex hormone estradiol, due to menstrual fluctuations or hormonal contraceptive use. As fear extinction is a laboratory model of exposure therapy for anxiety and trauma disorders, here we assessed the hypothesis that treatment outcomes may be diminished when exposure therapy occurs during periods of low estradiol. 90 women with spider phobia (60 cycling and 30 using hormonal contraceptives) underwent a one-session exposure treatment for spider phobia, following which, serum estradiol levels were assessed. A median split in estradiol level was used to divide cycling participants into two groups; lower and higher estradiol. Behavioral avoidance and self-reported fear of spiders were measured pre-treatment, post-treatment, and at a 12 week follow-up assessment. Women using hormonal contraceptives exhibited a significantly slower rate of improvement across treatment, greater behavioral avoidance at post-treatment and follow-up, and fewer self-initiated post-treatment exposure tasks, relative to both groups of cycling women, who did not differ. No group differences in self-reported fear were evident. Correlational analyses revealed that across the whole sample, lower estradiol levels were associated with slower rates of improvement across treatment, and greater self-reported fear and behavioral avoidance at post-treatment, but not follow-up. These results provide the first evidence of an association between endogenous estradiol, hormonal contraceptive use, and exposure therapy outcomes in spider phobic women. Hormonal profile may partly account for variability in responsiveness to psychological treatments for anxiety and trauma disorders in women.

The present study assessed the circumstances under which size estimation biases in spider phobia occur, and whether such biases are modifiable by treatment. Women with (n = 67) and without (n = 33) spider phobia approached a spider during a behavioral approach test (BAT). They provided size estimates of the spider both during and shortly after the BAT (with the spider in view, or not in view, respectively). Phobic women then received cognitive therapy or a placebo treatment and one week later they underwent a second BAT and provided size estimates of the same spider during and after the BAT. Phobic women reported larger size estimates than non-phobic women after, but not during, the BAT. Size estimates after, but not during, the BAT correlated with self-reported fear but not avoidance. Size estimates after, but not during, the BAT reduced from the first to second BAT in phobic women; an effect evident in both the cognitive therapy and placebo treatment conditions. Changes in size estimates were not associated with treatment-induced reductions in fear or avoidance. These results suggest that estimation biases in spider phobia are likely driven by non-perceptual processes. The clinical utility of size estimation measures is discussed.

Summary Increased prevalence, severity, and burden of anxiety, trauma-related and stress-related disorders in women compared with men has been well documented. Evidence from a variety of fields has emerged suggesting that sex hormones, particularly oestradiol and progesterone, play a significant part in generation of these sex differences. In this Series paper, we aim to integrate the literature reporting on the effects of sex hormones on biological, behavioural, and cognitive pathways, to propose two broad mechanisms by which oestradiol and progesterone influence sex differences in anxiety disorders: augmentation of vulnerability factors associated with anxiety disorder development; and facilitation of the maintenance of anxious symptoms post-development. The implications for future research, along with novel approaches to psychological and pharmacological treatment of anxiety disorders, are also considered.

Many people with traumatic brain injury (TBI) have poor emotion recognition, with negative emotions more frequently impaired. They can also display abnormal affective responses to emotionally charged material, however, the mechanisms underpinning such deficits are unclear. This study examined whether affective responsivity can be improved by focusing attention and whether responsivity is associated with perception accuracy. Eighteen adults with moderate-to-severe TBI and 18 control participants viewed facial expressions while skin conductance (SCR) and evoked cardiac deceleration (ECD) (used as indices of orientation) and skin conductance levels (SCL) (used as an index of phasic arousal) were monitored. They viewed two blocks of faces (8 angry and 8 happy per block), passively in the first block and with the instruction to identify the emotional expression in the second. No differences between conditions, emotions or groups were found using SCR. Both groups demonstrated increasing ECD for the attend condition relative to the passive condition. For the passive task the control group showed increasing SCL (sensitisation) over trials when viewing angry faces and decreasing SCL (habituation) to happy faces. No differences between emotions were shown for the TBI group who rapidly habituated to both expressions. For the attend task, there was no evidence of habituation for either expression for either the control or TBI participants. Physiological measures did not correlate to accuracy in recognising emotions. The results suggest that increasing attentional demands improves orientation and emotional engagement (arousal) to emotional faces following TBI. However, the relationship to this and emotion perception accuracy remains unclear.