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. Author manuscript; available in PMC: 2022 May 6.
Published in final edited form as: Arch Womens Ment Health. 2014 Oct 1;18(2):239–246. doi: 10.1007/s00737-014-0456-1

The role of perceived control over anxiety in prospective symptom reports across the menstrual cycle

Jennifer N Mahon 1, Kelly J Rohan 2, Yael I Nillni 3, Michael J Zvolensky 4
PMCID: PMC9074117  NIHMSID: NIHMS1791295  PMID: 25269759

Abstract

The present investigation tested the role of psychological vulnerabilities to anxiety in reported menstrual symptom severity. Specifically, the current study tested the incremental validity of perceived control over anxiety-related events in predicting menstrual symptom severity, controlling for the effect of anxiety sensitivity, a documented contributor to menstrual distress. It was expected that women with lower perceived control over anxiety-related events would report greater menstrual symptom severity, particularly in the premenstrual phase. A sample of 49 normally menstruating women, aged 18–47 years, each prospectively tracked their menstrual symptoms for one cycle and completed the Anxiety Control Questionnaire (Rapee, Craske, Brown, & Barlow Behav Ther 27:279–293. doi:10.1016/S0005-7894(96)80018-9, 1996) in their follicular and premenstrual phases. A mixed model analysis revealed perceived control over anxiety-related events was a more prominent predictor of menstrual symptom severity than anxiety sensitivity, regardless of the current cycle phase. This finding provides preliminary evidence that perceived control over anxiety-related events is associated with the perceived intensity of menstrual symptoms. This finding highlights the role of psychological vulnerabilities in menstrual distress. Future research should examine whether psychological interventions that target cognitive vulnerabilities to anxiety may help reduce severe menstrual distress.

Keywords: Perceived control, Anxiety sensitivity, Premenstrual symptoms, Menstrual cycle

Introduction

Significance

Premenstrual distress is very common, with 90% of women reporting physiological and psychological symptoms associated with the premenstrual, or late luteal, menstrual phase (Strine et al. 2005; Yonkers et al. 2003). Commonly reported premenstrual symptoms include tension, dysphoria, irritability, pain, impaired concentration, headaches, fatigue, and insomnia (Chrisler and Caplan 2002; Halbreich et al. 2003; Logue and Moos 1986; Yonkers et al. 2003). The premenstrual phase is associated with exacerbations of mood and anxiety disorders such as major depression (Kornstein et al. 2008), premenstrual dysphoric disorder (PMDD; Yonkers et al. 2003), and panic disorder (Breier et al. 1986; Cook et al. 1990; Kaspi et al. 1994). The premenstrual phase also poses notable problems for subclinical and even nonclinical populations, for whom the premenstrual phase is associated with functional impairments in sleep and pain as well as increases in depression and anxiety (Gonda et al. 2008; Strine et al. 2005; Yonkers et al. 2003).

Theory and background

The inter-individual variation in premenstrual symptom severity may relate to individual biological and psychological vulnerabilities. The menstrual reactivity hypothesis (Sigmon et al. 2000c) is a diathesis-stress model that proposes cognitive vulnerabilities to anxiety and depression (i.e., the psychological diathesis) interact with hormonal fluctuations during the menstrual cycle, particularly in the premenstrual phase (i.e., the biological stress) to influence the severity of menstrual symptoms. Heilbrun and Rener (1988) found that nonclinical, normally menstruating women tended to identify the onset of menstruation as an unavoidable stressor, which suggests that even for nonclinical women with regular cycle lengths, the premenstrual phase can be identified as reliably stressful.

In terms of candidate cognitive risk factors that may constitute the diathesis, locus of control has been implicated in premenstrual distress. An initial study examining the association between menstrual symptom severity and locus of control (per the Levenson LOC scale; Levenson 1981) in normally menstruating women found that women assessed in the premenstrual phase reported a lower internal locus of control relative to women assessed in the follicular phase, and externality of reported locus of control in the premenstrual phase was associated with greater reported premenstrual symptom severity. However, this study was limited by retrospective reports of premenstrual distress and a cross-sectional sample. Two longitudinal examinations of locus of control across menstrual phases using Rotter’s I-E scale found that women who reported a greater severity of premenstrual symptoms also reported an increased external locus of control in the premenstrual phase relative to themselves at other menstrual phases, and relative to women who reported the overall lower premenstrual symptom severity (Christensen et al. 1992; O’Boyle et al. 1988). In contrast, a third longitudinal study testing the relation of locus of control, as measured by Rotter’s I-E Scale and a clinically derived scale, and premenstrual symptom severity in a sample of normally menstruating women did not show a fluctuation in locus of control across menstrual phases (Martin 1999).

There are a variety of possible reasons for the inconclusive literature on locus of control-menstrual symptom relations. First, the lack of convergent findings regarding the association between locus of control and menstrual symptoms may be due to the measurement of global locus of control, nonspecific to stress or anxiety. These prior studies have used measures reflecting a global perception of causality in one’s life, based on the definition by Rotter (1966). Conversely, Barlow (2002) conceptualizes anxiety as involving a sense of uncontrollability over potentially threatening events and negative emotions, with control defined as the ability to influence events and outcomes in one’s environment (Chorpita & Barlow 1998). Lower perceived control over threatening stimuli is associated with anxious arousal, apprehension, and uncertainty about coping. Consistent with the influential perspective forwarded by Barlow (2002), numerous experimental laboratory-based studies have indicated that persons who lack, or have lost, the perceived ability to terminate exposure to aversive bodily sensations report greater anxiety and panic symptoms than their counterparts who do not lack such perceived control (Sanderson et al. 1989; Telch 1996; Zvolensky et al. 1999; Zvolensky et al. 1998).

Researchers have conceptualized lower perceived control over a threat as a shared diathesis for anxiety and depression (Alloy et al. 1990; Barlow 2002). As common menstrual symptoms overlap with anxiety and mood symptoms (e.g., irritability, dysphoria, impaired concentration, fatigue, insomnia, tension, headaches, and pain; Strine et al. 2005), perceived control, as conceptualized by Barlow and colleagues and found to be more central to anxiety and depression, may therefore be more pertinent to the experience of menstrual symptoms. Rapee et al. (1996) developed the Anxiety Control Questionnaire (ACQ) as a specific measure of perceived control to anxiety-related events. Specifically, the ACQ was designed to measure trait-like individual differences in perceived control over internal and external events/situations that are relevant to anxiety and its disorders (Brown et al. 2004; Zebb and Moore 1996; Rapee et al. 1996). Perceived control over anxiety-related events, as measured by the ACQ, is concurrently related to agoraphobic avoidance among persons with panic disorder (White et al. 2006) and panic-relevant interpretative biases for threat among nonclinical individuals (Zvolensky et al. 2001). Although the ACQ has not always been predictive of panic responsivity (e.g., Gregor and Zvolensky 2008), it is possible trait-like perceptions of control over anxiety-related events is relevant to menstrual symptom expression.

Second, the current literature examining perceived control as a contributing factor to menstrual distress has largely utilized cross-sectional designs rather than longitudinal designs that allow for a more robust repeated measure test controlling for baseline values and other within-subject variability. Thus, the covariation of cycle fluctuation in perceived control and menstrual symptom reporting within individuals was not considered in the previous work.

Third, no study examining the effect of perceived control over anxiety-related events across the menstrual cycle has controlled for the effect of anxiety sensitivity (AS), which has been shown to predict menstrual symptoms (Nillni et al. 2013; Sigmon et al. 1996, 2000a, b), and to serve as a cognitive vulnerability in the diathesis-stress model (Nillni et al. in press; Sigmon et al. 2000c). AS is the fear of anxiety, anxiety-related bodily sensations, and their consequences (Reiss and McNally 1985); individuals high in AS tend to be hypervigilant to physiological arousal and to misinterpret arousal sensations as dangerous. Given the similarity between anxiety sensations and menstrual symptoms, Sigmon et al. (1996; 2000a, b) tested whether AS also predicted menstrual distress and found that women high in AS reported greater menstrual symptoms across the cycle as compared to low-AS women. Thus, AS appears to be part of the diathesis for enhanced menstrual symptom severity and could represent a potential confound in the previously reported effects of perceived control on menstrual distress.

Lastly, results regarding perceived control and menstrual distress may be mixed and inconclusive due to limitations of menstrual phase estimation. Lane and Francis (2003) employed participants’ retrospective recall of the timing of their prior menstrual phase. Martin (1999) assessed the menstrual phase by restricted day count: follicular (day 9), luteal (day 20), and premenstrual (day 26). However, Shirtcliff et al. (2001) reported typical discrepancies between menstrual cycle estimation methods and concluded that menstrual day count alone matched the correct menstrual phase only about 50% of the time when later verified by progesterone assay. Thus, these different methodological approaches to defining cycle phase status have greatly limited prior studies.

Together, the current study aimed to address these limitations by using a prospective, longitudinal design to examine whether perceived control specific to anxiety-related events is implicated in premenstrual distress in normally menstruating women. Specifically, the study tested whether (1) perceived control over anxiety-related events fluctuated between the follicular and premenstrual phases within normally mentruating women and (2) perceived control over anxiety-related events interacts with menstrual phase to specifically predict premenstrual symptom severity, after controlling for AS. It was expected that women would generally report lower perceived control over anxiety in the premenstrual phase relative to the follicular phase and that lower perceived control over anxiety would predict variation in menstrual symptom severity across menstrual phases, even when controlling for AS.

Materials and methods

Participants

The current study was part of a larger study examining panic responses across the menstrual cycle (Nillni et al. 2012) conducted in the Department of Psychology at the University of Vermont. A total of 65 healthy, normally menstruating women (i.e., average cycle length of 25–35 days that did not regularly vary in length month to month by ≥7 days) initially enrolled in the parent study. The 49 women who completed the prospective daily menstrual symptom tracking over at least one menstrual cycle were included in these longitudinal analyses. In this sample of 49, participants ranged in age from 18 to 47 years (M=26.20, SD=9.13). The sample characteristics were as follows: 4% identified as Hispanic, 86% Caucasian, 4% as American Indian, 4% as Asian, 4% as African American, and 2% as other; 69% reported a single marital status. Prior to participation, participants were informed of the study procedures and risks. This research was approved by the Institutional Review Board at the University of Vermont.

Measures

Anxiety Control Questionnaire 15-item version

The ACQ (Rapee et al. 1996) was developed to measure an individual’s perceived control over anxiety and anxiety-related events. Participants rate their level of agreement on a 6-point Likert scale (0=“strongly disagree” to 5=“strongly agree”) for 15 perceived control statements (e.g., “Most events that make me anxious are outside my control”). A confirmatory factor analysis revealed a higher-order factor of perceived control comprised of a 3-factor lower-order solution (emotion control, threat control, and stress control; loadings=.70, .72, .86, respectively; p<.001); all three subscales demonstrated scale reliabilities acceptable in clinical and nonclinical samples (α=.65–.74; Brown et al. 2004). The emotion control subscale measures the perceived ability to control one’s emotions (e.g., “I am able to control my level of anxiety”); the threat control subscale assesses the perceived ability to escape from frightening events (e.g., “There is little I can do to change frightening events”); the stress control subscale measures the perceived difficulty coping in stressful situations (e.g., “When I am put under stress, I am likely to lose control”). The total score of the 15-item ACQ (range=0–75) was utilized in the present study as a measure of global perceived control for anxiety-related events. The ACQ demonstrated good internal consistency in the current sample in both the follicular and premenstrual phases (α=.86, α=.89, respectively).

Anxiety sensitivity index

The anxiety sensitivity index (ASI) (Reiss and McNally 1985; Reiss et al. 1986) is a 16-item self-report measure of fear of bodily sensations related to anxious arousal. Individuals rate statements (e.g., “It scares me when I feel shaky”) on a 5-point Likert scale (0=“very little” to 4=“very much”), indicating the degree to which they worry about possible consequences of anxiety symptoms. The total score, the sum of all items (range=0–64), represents the global-order AS factor. The ASI has demonstrated acceptable test-retest reliability (.71–.75) and validity and good internal reliability (α=.88) (Peterson and Heilbronner 1987; Reiss et al. 1986). The 16-item ASI has been used in all past studies examining AS, menstrual cycle phase, and menstrual distress (Sigmon et al. 1996, 2000a, b, c). Given that AS is considered as a relatively stable factor, the ASI was completed at the screening visit only. The ASI demonstrated good internal consistency in the current sample (α=.78).

Daily Record of Severity of Problems

The Daily Record of Severity of Problems (DRSP) (Endicott et al. 2006) is a 14-item daily questionnaire that measures severity of physical and psychological symptoms (e.g., “felt angry, irritable”) across the menstrual cycle, including three impairment items scored on a 6-point Likert scale (1=“not at all” to 6=“extreme”). The DRSP has been shown to be a reliable and valid measure for identification of premenstrual symptoms and impairment (Endicott et al. 2006). Participants completed this questionnaire daily throughout the study duration (≥one full menstrual cycle). All items were summed to create a daily score.

Screening procedures

Participants completed a screening visit consisting of a diagnostic interview with the Structured Clinical Interview for DSM-IV Axis I Disorders —Non-patient version (First et al. 1994) and a medical questionnaire to assess inclusion/exclusion criteria. Participants were excluded from the study due to (1) menopausal status; (2) current use of a hormonal contraceptive; (3) pregnancy (based on self-report); (4) any current anxiety disorder, alcohol or substance dependence, or past panic disorder with or without agoraphobia, determined by the SCID-NP (First et al. 1994); (5) acute and serious suicidal intent; (6) seizure disorder; (7) asthma or respiratory problems; (8) current use of anxiolytic medication; and (9) reporting irregular menstrual cycles or an average menstrual cycle length that fall outside the norm for most women of 25–35 days.

Laboratory visit procedures

The study included two laboratory visits, one during the premenstrual phase and one during the follicular phase of the menstrual cycle. To eliminate procedural bias of the study order, the initial cycle phase of testing (i.e., premenstrual or follicular first) was randomly assigned using a pre-generated list of random permuted blocks of sizes 6 and 8. At each visit, participants completed the Anxiety Control Questionnaire (ACQ; Rapee et al. 1996) and provided a saliva sample via passive drool (Salimetrics 2010).

Scheduling of laboratory visits and ovulation testing

Participants notified the research staff of the day 1 of their menses following the screening visit. The premenstrual phase was defined as the 5 days prior to menstruation onset, and the follicular phase was defined as days 6–12 of the cycle. These day ranges are based on a 28-day cycle and were adjusted for women with other normal cycle lengths (Asso 1983). As the luteal phase duration can vary within an individual, at-home ovulation testing was completed to verify the day of peak in luteinizing hormone (LH), after which ovulation should occur within 48 h. Ovulation testing dates were determined by average menstrual cycle length (e.g., daily testing began on day 12 for a 28-day average cycle). Participants were informed to notify the research staff when a positive LH peak was detected. The participants were subsequently scheduled for the premenstrual visit, 12–14 days following the LH peak. Thus, the LH peak was utilized in combination with estimated cycle length to prospectively predict the occurrence of the premenstrual phase in order to reduce the amount of lost data due to the low agreement between day count estimation and progesterone assay (~50%, Shirtcliff et al. 2001).

Cycle phase verification

Menstrual cycle phase was later verified by salivary assay of progesterone for inclusion in the data analysis. The samples were stored at −40 °C and sent to Salimetrics, LLC within 2 months for progesterone enzyme immunoassay. On the day of the assay, the specimens were thawed completely, vortexed, and centrifuged; the assay range was >1 pg/ml. Phase verification was based on progesterone means reported in normally menstruating women (follicular: 80.35 pg/ml, SD=34.8; premenstrual: 136.30 pg/ml, SD=82.3). However, normal variation in progesterone concentration was expected due to assessment timing as progesterone and inter-individual variation in the rate of progesterone decline across the premenstrual phase (Rubinow et al. 1988). Therefore, day count, ovulation, and progesterone were utilized in conjunction to inform phase verification such that menstrual cycle start date and LH peak and were used as primary measures of cycle estimation whereas progesterone level was used as a secondary measure of verification. The follicular phase was considered verified if a positive peak in LH was detected following the follicular laboratory visit or progesterone level was within ±1 SD of mean. The premenstrual phase visit was considered verified if menstruation began within 5 days following the premenstrual lab visit; there was an LH peak detected prior to the visit, or progesterone level was within ±1 SD of mean.

Results

Premenstrual vs. follicular phase differences in perceived control over anxiety

A paired-sample t test (two-tailed) was used to examine whether perceived control to anxiety-related events on the ACQ fluctuates between the premenstrual vs. follicular phases of the menstrual cycle. As the ACQ was administered at two time points, estimated to be in different menstrual cycle phases, within-subject analyses to test for phase differences in the ACQ included a smaller subset of women (n=38, 78% of the total sample) for whom both the follicular and premenstrual menstrual phases were confirmed based on the above criteria. Ratings of perceived control over anxiety-related events did not significantly differ between phases [t (37)= −1.49, p=.144], and the ratings appeared quite stable across phases (follicular: M=48.26, SD=10.01; premenstrual: M=49.45, SD=11.11). Of the 38 women, 14 (29%) met DRSP criteria for a clinically significant premenstrual symptom severity (PMS), as measured by a greater mean severity of symptoms in the premenstrual phase relative to the follicular phase and by clinical severity rating of at least 5 for at least one symptom in the premenstrual phase (Borenstein et al. 2007). A series of paired sample t tests also examined variation in the ACQ (total and subscale scores) across phases in the women who met for PMS and for whom both phases were also confirmed (N= 11). None of the ACQ scores demonstrated differences across phase; ACQ total score, t (10)=−.69, p=.501; EC, t (10)=−.96, p=.359; TC, t (10)=.70, p=.500; and SC, t (10)=−.78, p=.455. The current findings are consistent with the research suggesting that the ACQ demonstrates stability across time and supports the construct validity of the ACQ as a measure of trait perceived control over anxiety-related events (Rapee et al. 1996).

Perceived control over anxiety and anxiety sensitivity as predictors of menstrual symptoms

In order to examine symptom change across menstrual cycles, only women who completed the DRSP for at least one menstrual cycle were included in this analysis (n=49). To delineate distinct menstrual symptom severity outcomes for each phase of interest, all available days of DRSP data were averaged for each participant, separately during the follicular and premenstrual phases. The mean follicular and premenstrual DRSP outcome variables were then transformed using logarithmic transformation as the raw values were significantly skewed (follicular: skewness=1.36, standard error (SE)=0.34; premenstrual: skewness=1.77, SE=0.34). The transformation skewness coefficients were improved (follicular: skewness=0.63, SE=0.34; premenstrual: skewness=0.45, SE=0.34). A paired t test on log-transformed DRSP outcomes revealed a greater menstrual symptom severity in the premenstrual phase (M=1.40, SD=0.15) relative to the follicular phase (M=1.31, SD=0.12), t (48)=−5.58, p=.001, d=0.64.

Zero-order correlations were computed among variables. The follicular ACQ rating was highly correlated with the premenstrual ACQ rating (r=0.90, p <.001), indicative of possible collinearity. Thus, for the subsequent analysis in which ACQ was tested in a linear mixed model on DRSP ratings, the ACQ completed at the first assessment for each participant (randomly assigned) was entered as a trait predictor.

Linear mixed modeling was utilized to test whether perceived control over anxiety (ACQ) interacted with menstrual cycle phase (time; premenstrual, follicular) in the prediction of menstrual symptom severity on the DRSP. It was hypothesized that the perceived control × phase interaction would be significant, such that lower perceived control on the ACQ would predict the change in menstrual symptom severity from the follicular to the premenstrual phase. Sequential modeling was utilized to test the effects.

In model 1, perceived control to anxiety-related events (ACQ score) was entered as a fixed predictor with phase as the time variable. The interaction of perceived control and phase was also entered. In model 1, there was a significant main effect of ACQ on menstrual symptom severity (DRSP score), F (1, 46)=14.67, p<.001; such that ACQ significantly predicted menstrual symptom severity, regardless of phase. The negative gradient (b=−.006, t (46)=−3.51, p=.001) that indicates lower perceived control predicted a greater menstrual symptom severity. Phase was also a significant predictor of menstrual severity [F (1, 46)=5.08, p=.029], reflecting greater menstrual symptom severity in the premenstrual phase relative to the follicular phase, as reported in the paired t test on the DRSP above. However, the interaction of perceived control and phase was ns, F (1, 46)=1.00, p=.322, indicating perceived control did not uniquely predict individual change in DRSP between phases.

In model 2, AS replaced perceived control as the fixed predictor such that AS, phase, and the AS × phase interaction were entered into the model. As illustrated in our previous report (Nillni et al. 2013), the main effect of AS on menstrual symptom severity was significant, F (1, 47)=11.39, p=.001, η2=.195, showing that ASI predicted menstrual symptom severity, regardless of phase. The positive coefficient (b=.009, t (47)=2.89, p=.006) indicates higher AS predicted a greater menstrual symptom severity. The main effect of phase was ns in model 2, F (1, 47)=−2.00, p=.052. The interaction of AS and phase was also ns, indicating that, similar to perceived control, AS did not predict individual change in menstrual severity across time (between menstrual phases), F (1, 47)=.16, p=.695.

Model 3 involved both perceived control and AS as independent fixed predictors, phase, and the interaction of ACQ × phase. This model was used to test whether the unique main effects of AS and perceived control remained significant when jointly entered into the model, see Table 1. When controlling for the main effect of AS, the main effect of perceived control over anxiety remained significant, F (1, 46.65)=5.53, p=.023, η2=.242. Therefore, lower perceived control remained a significant predictor of menstrual symptom severity, regardless of phase, even after controlling for AS. Phase also remained significant, F(1, 46)=5.08, p=.029, η2=.099. Interestingly, the main effect of AS was no longer significant when perceived control was included in the model, F (1, 45)=2.58, p=.115, indicating that perceived control may be a stronger predictor of the overall menstrual symptom distress than AS. The shared variance of AS (total score measured at the screening visit) and ACQ (total score measured within each phase) was r2=.312 and r2=.300 for the follicular and premenstrual phases, respectively. The interaction of perceived control x phase also remained ns in model 3, F (1, 46)=1.00, p=.322, indicating that perceived control was a significant predictor of menstrual distress experienced across phases.

Table 1.

Linear mixed modeling results for DRSP menstrual symptom severity in the premenstrual and follicular phases

B SE t p
ACQ −.01 .00 −2.36 .02
ASI   .00 .00   1.61 .12
Phase −.16 .07 −2.25 .03
ACQ × phase   .00 .00   1.00 .32

DRSP Daily Record of Severity of Problems (Endicott et al. 2006), ACQ Anxiety Control Questionnaire (Rapee et al. 1996), ASI anxiety sensitivity index total score (Reiss and McNally 1985; Reiss et al. 1986), phase=premenstrual vs. follicular menstrual cycle phase

Model 3 was also run with each of the three ACQ subscale scores entered as the predictor variable, controlling for AS, to explore the relative contributions of perceived control as specific to emotions, stress, or threat within the observed overall pattern of results. The threat control and stress control subscale scores were nonsignificant predictors of menstrual symptom severity when controlling for AS (p=.338 and p=.098, respectively). However, emotion control emerged as a significant predictor of overall menstrual symptom severity, F (1, 46)=9.25, p=.004, and AS became nonsignificant in the joint model, F (1, 45)=2.35, p=.132, η2=.295. Therefore, the ACQ emotion control subscale showed the same pattern of results as the total ACQ score. The shared variance of AS (total score measured at the screening visit) and ACQ emotion control (subscale score assessed in each phase) was r2=.276 and r2=.201 for the follicular and premenstrual phases, respectively.

Discussion

Results interpretation

The current study measured both perceived control over anxiety and AS and collected daily menstrual symptom severity ratings to investigate whether these psychological constructs were related to the menstrual phase and menstrual symptom severity reported across phases.

The study compared relative predictive effects of perceived control vs. AS on menstrual symptoms in the premenstrual and follicular phases. The current findings support the role of lower perceived control over anxiety-related events as a significant contributing factor to menstrual symptomatology. This effect was nonspecific to the current cycle phase, as menstrual symptoms were more severe in the premenstrual than in the follicular phase; neither perceived control over anxiety nor AS predicted change in symptoms between the two phases. Although both perceived control over anxiety and AS exhibited main effects on menstrual symptom severity, regardless of the current cycle phase, only the unique effect of perceived control remained significant in the joint model. This finding suggests that perceived control over anxiety-related events predicted variance in menstrual symptom severity above and beyond the effect of AS, and that perceived control over anxiety-related events may be a stronger predictor of menstrual symptom severity than AS. To our knowledge, prior studies on psychological risk factors for menstrual symptoms have not included the Anxiety Control Questionnaire (ACQ; Rapee et al. 1996) and have not compared the predictive power of perceived control specific to anxiety and AS in predicting menstrual symptoms. The nonsignificant main effect of AS in the joint model was unexpected given the overlap of anxiety-related sensations and menstrual symptoms. For this reason, these findings require replication in future studies. The predictive pattern of the overall ACQ was replicated with the ACQ emotion control subscale, indicating that women with lower perceived control specific to their experienced anxious emotion report greater severity of menstrual symptoms across phases.

Contrary to our hypotheses, perceived control over anxiety-related events did not differ between the premenstrual and follicular phases. This finding is inconsistent with the past research on locus of control, which found that women report lower internal locus of control in the premenstrual phase. However, the current study demonstrates the stability of the ACQ across the menstrual cycle, consistent with the conceptualization of the ACQ as a trait measure of perceived control over anxiety-related events (Rapee et al. 1996).

The current findings suggests that women who are generally lower in perceived control over anxiety-related events (and specifically over their experienced anxiety), as well as those who are generally higher in AS, may be prone to report a greater menstrual symptom severity at all times. As lower perceived control over anxiety-related events is a general risk factor for anxiety and depression (Barlow 2002), it may be that perceived control is predicting the overlap of symptoms pertaining to anxiety, depression, and menstrual symptoms (i.e., a common negative affectivity construct), and that other factors may contribute to the symptom fluctuation across phases. The contribution of lower perceived control over anxiety-related events to reported menstrual distress is noteworthy as it highlights the role of psychological vulnerabilities in experienced menstrual (i.e., physical) distress. Future research should examine whether lower perceived control is also a significant contributor to clinical levels of menstrual symptoms and whether clinical menstrual syndromes such as PMS or PMDD may be effectively ameliorated with psychological interventions that target cognitive vulnerabilities specific to anxiety.

Limitations

The current study design has several noteworthy limitations. First, the study did not include a measure of general internal vs. external locus of control for comparison to the existing literature. A meaningful analysis for future studies would compare whether global locus of control and perceived control over anxiety comparably or differentially predict menstrual symptoms. Second, the current design did not include a state measure of perceived control over anxiety. Given that the ACQ has shown stability across time and is intended to measure trait perceived control, examining whether state perceived control varies across menstrual phases would have added strength to the study. Third, the current sample presented with a relatively low menstrual symptom severity in both the follicular (median=20.20) and premenstrual (median=23.67) phases on a possible DRSP scale range of 14–84. The effect of perceived control over anxiety-related events may be more pronounced in women with more severe menstrual distress, consistent with prior research suggesting a greater effect of locus of control in women who meet the criteria for PMS or PMDD than nonclinical controls (O’Boyle et al. 1988; Smith and Thomas 1996). Lastly, the population was primarily Caucasian (86%), so it may be that these results may be limited in generalizability to the broader, ethnically diverse population.

The current study examined perceived control over anxiety-related events as it pertains to menstrual symptoms in women with regular, normal menstrual cycle lengths (25–35 days). Given that lower perceived control involves perceived uncontrollability of emotions in reaction to threat and stress, future research should explore whether perceived control to anxiety influences menstrual symptoms in women with irregular menstrual cycles, in whom menstrual symptoms are less predictable. Additionally, women who have experienced a repeated pairing of premenstrual symptoms and clinically significant emotional distress, as in PMDD, may be more vulnerable to lower perceived control to anxiety-related events in the premenstrual phase. This would build upon prior literature suggesting women with more severe menstrual symptoms report a lower internal locus of control (Christensen et al. 1992; O’Boyle et al. 1988). Thus, research examining state perceived control measures in clinical populations may provide more information on menstrual cycle-specific psychological factors contributing to premenstrual distress.

Conclusions

This study examined the interaction of perceived control over anxiety and the current menstrual cycle phase on menstrual symptoms. The findings suggest that lower perceived control over anxiety is a unique predictor of menstrual distress, regardless of current phase, even after controlling for the effect of AS. The significantly diminished effect of AS on menstrual symptom severity with perceived control included in the model suggests that lower perceived control may be a stronger predictor of menstrual symptom distress than higher AS. Given that women are at least twice as prone to experience clinical anxiety and depression as men, future studies should further examine the interplay between psychological and biological factors to better understand the profiles of risk for mood and anxiety disorders that fluctuate in severity with the menstrual cycle.

Acknowledgments

This project was conducted as part of a larger study funded under Yael I. Nillni by the National Institute of Mental Health—1R36MH086170-01A1.

Footnotes

Conflict of interest The authors declare that they have no conflict of interest.

Contributor Information

Jennifer N. Mahon, Department of Psychology, University of Vermont, John Dewey Hall, 2 Colchester Avenue, Burlington, VT 05405-0134, USA

Kelly J. Rohan, Department of Psychology, University of Vermont, John Dewey Hall, 2 Colchester Avenue, Burlington, VT 05405-0134, USA

Yael I. Nillni, Department of Psychology, University of Vermont, John Dewey Hall, 2 Colchester Avenue, Burlington, VT 05405-0134, USA; National Center for PTSD, Women’s Health Sciences Division, VA Boston Healthcare System, 150 South Huntington Avenue (116B-3), Boston, MA 02130-4817, USA; Boston University School of Medicine, Boston, MA, USA

Michael J. Zvolensky, University of Houston, Heyne Building Room 129, 4800 Calhoun Road, Houston, TX 77004-5022, USA; MD Anderson Cancer Center, Department of Behavioral Science, The University of Texas, Austin, TX, USA

References

  1. Alloy LB, Kelly KA, Mineka S, Clements CM (1990) Comorbidity of anxiety and depressive disorders: a helplessness-hopelessness perspective. In: Maser JD, Cloniger CR (eds) Comorbidity of mood and anxiety disorders. American Psychiatric Association, Washington DC, pp 499–543 [Google Scholar]
  2. Asso D (1983) The real menstrual cycle. John Wiley & Sons, New York [Google Scholar]
  3. Barlow DH (2002) Anxiety and its disorders: the nature and treatment of anxiety and panic, 2nd edn. The Guildford Press, New York [Google Scholar]
  4. Borenstein JE, Dean BB, Leifke E, Korner P, Yonkers KA (2007) Differences in symptom scores and health outcomes in premenstrual syndrome. J Women’s Health 16:1139–1144 [DOI] [PubMed] [Google Scholar]
  5. Breier A, Charney DS, Heninger GR (1986) Agoraphobia with panic attacks: development, diagnostic stability, and course of illness. Arch Gen Psychiatr 43:1029–1036 [DOI] [PubMed] [Google Scholar]
  6. Brown TA, White KS, Forsyth JP, Barlow DH (2004) The structure of perceived emotional control: psychometric properties of a revised anxiety control questionnaire. Behav Ther 35:75–99. doi: 10.1016/S0005-7894(04)80005-4 [DOI] [Google Scholar]
  7. Chorpita BF, Barlow DH (1998) The development of anxiety: the role of control in the early environment. Psychol Bull 124:3–21. doi: 10.1037/0033-2909.124.1.3 [DOI] [PubMed] [Google Scholar]
  8. Chrisler JC, Caplan P (2002) The strange case of Dr. Jekyll and Ms. Hyde: how PMS became a cultural phenomenon and a psychiatric disorder. Annu Rev Sex Res 13:274–306. doi: 10.1080/10532528.2002.10559807 [DOI] [PubMed] [Google Scholar]
  9. Christensen AP, Board BJ, Oei TP (1992) A psychosocial profile of women with premenstrual dysphoria. J Affect Disorders 25:251–259 [DOI] [PubMed] [Google Scholar]
  10. Cook BL, Noyes R, Garvey MJ, Beach V, Sobotka J, Chaudhry D (1990) Anxiety and the menstrual cycle in panic disorder. J Affect Disorders 19:221–226. doi: 10.1016/0165-0327(90)90095-P [DOI] [PubMed] [Google Scholar]
  11. Endicott J, Nee J, Harrison W (2006) Daily Record of Severity of Problems (DRSP): reliability and validity. Arch Wom Ment Health 9:41–49. doi: 10.1007/s00737-005-0103-y [DOI] [PubMed] [Google Scholar]
  12. First M, Spitzer R, Gibbon M, Williams J (1994) Structured Clinical Interview for DSM-IV Axis I Disorders—non-patient edition. Biometrics Research Department, New York [Google Scholar]
  13. Gonda X, Telek T, Juhasz G, Lazary J, Vargha A, Bagby G (2008) Patterns of mood changes throughout the reproductive cycle in healthy women without premenstrual dysphoric disorders. Prog Neuro-Psychoph 32:1782–1788. doi: 10.1016/j.pnpbp.2008.07.016 [DOI] [PubMed] [Google Scholar]
  14. Gregor K, Zvolensky MJ (2008) Anxiety sensitivity and perceived control over anxiety-related events: evaluating the singular and interactive effects in the prediction of anxious and fearful responding to bodily sensations. Behav Res Ther 46:1017–1025 [DOI] [PubMed] [Google Scholar]
  15. Halbreich U (2003) The etiology, biology, and evolving pathology of premenstrual syndromes. Psychoneuroendocrino 28:55–99. doi: 10.1016/S0306-4530(03)00097-0 [DOI] [PubMed] [Google Scholar]
  16. Heilbrun AB Jr, Rener D (1988) Psychological defenses and menstrual distress. Brit J Med Psychol 61:219–230. doi: 10.1111/j.2044-8341.1988.tb02783.x [DOI] [PubMed] [Google Scholar]
  17. Kaspi SP, Otto MW, Pollack MH, Eppinger S, Rosenbaum JF (1994) Premenstrual exacerbation of symptoms in women with panic disorder. J Anxiety Disord 8:131–138. doi: 10.1016/0887-6185(94)90011-6 [DOI] [Google Scholar]
  18. Kornstein SG, Harvey AT, Rush AJ, Wisniewski SR, Trivedi MH, Svikis DS, McKenzie ND, Bryan C, Harley R (2008) Self-reported premenstrual exacerbation of depressive symptoms in patients seeking treatment for major depression. Psychol Med 35:683–692. doi: 10.1017/S0033291704004106 [DOI] [PubMed] [Google Scholar]
  19. Lane T, Francis A (2003) Premenstrual symptomatology, locus of control, anxiety and depression in women with normal menstrual cycles. Arch Wom Ment Health 6:127–138. doi: 10.1007/s00737-003-0165-7 [DOI] [PubMed] [Google Scholar]
  20. Levenson H (1981) Differentiating among internality, powerful others, and chance. In: Lefcourt H (ed) Research with the locus of control construct. Academic, New York, pp 15–63 [Google Scholar]
  21. Logue CM, Moos RH (1986) Perimenstrual symptoms: prevalence and risk factors. Psychosom Med 48:388–414 [DOI] [PubMed] [Google Scholar]
  22. Martin CR (1999) Phasic influences on psychometric measures during the menstrual cycle: implications for the construct integrity of the locus of control dimension. Brit J Med Psychol 72:217–226. doi: 10.1348/000711299159961 [DOI] [PubMed] [Google Scholar]
  23. Nillni YI, Rohan KJ, Zvolensky MJ (2012) The role of menstrual cycle phase and anxiety sensitivity in catastrophic misinterpretation of physical symptoms during a CO2 challenge. Arch Wom Ment Health 15:413–422 [DOI] [PMC free article] [PubMed] [Google Scholar]
  24. Nillni YI, Rohan KJ, Mahon JN, Pineles SL, Zvolensky MJ (2013). The role of anxiety sensitivity in the experience of menstrual-related symptoms reported via daily diary. Psychiat Res, 210(2): 564–569. doi: 10.1016/j.psychres.2013.07.016. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. O’Boyle M, Severino SK, Hurt SW (1988) Premenstrual syndrome and locus of control. Int J Psychiat Med 18:67–74. doi: 10.2190/HMNX-9V7J-652X-PWJ4 [DOI] [PubMed] [Google Scholar]
  26. Peterson RA, Heilbronner RL (1987) The anxiety sensitivity index: construct validity and factor analytic structure. J Anxiety Disord 1: 117–121. doi: 10.1016/0887-6185(87)90002-8 [DOI] [Google Scholar]
  27. Rapee RM, Craske MG, Brown TA, Barlow DA (1996) Measurement of perceived control over anxiety-related events. Behav Ther 27:279–293. doi: 10.1016/S0005-7894(96)80018-9 [DOI] [Google Scholar]
  28. Reiss S, McNally RJ (1985) The expectancy model of fear. In: Reiss S, Bootzin RR (eds) Theoretical issues in behavior therapy. Academic, New York, pp 107–122 [Google Scholar]
  29. Reiss S, Peterson RA, Gursky DM, McNally RJ (1986) Anxiety sensitivity, anxiety frequency and the prediction of fearfulness. Behav Res Ther 24:1–8. doi: 10.1016/0005-7967(86)90143-9 [DOI] [PubMed] [Google Scholar]
  30. Rotter J (1966) Generalized expectancies for internal versus external control of reinforcements. Psychol Monogr 80:1–28. doi: 10.1037/h0092976 [DOI] [PubMed] [Google Scholar]
  31. Rubinow DR, Hoban MC, Grover GN, Galloway DS, Roy-Byrne P, Andersen R, Merriam GR (1988) Changes in plasma hormones across the menstrual cycle in patients with menstrually related mood disorder and in control subjects. Am J Obstet Gynecol 158:5–11 [DOI] [PubMed] [Google Scholar]
  32. Salimetrics (2010) Salivary progesterone enzyme immunoassay kit. State College, Pennsylvania [Google Scholar]
  33. Sanderson WC, Rapee RM, Barlow DH (1989) The influence of an illusion of control on panic attacks induced via inhalation of 5.5% carbon-dioxide enriched air. Arch Gen Psychiatr 46:157–162. doi: 10.1001/archpsyc.1989.01810020059010 [DOI] [PubMed] [Google Scholar]
  34. Shirtcliff EA, Reavis R, Overman WH, Granger DA (2001) Measurement of gonadal hormones in dried blood spots versus serum: verification of menstrual cycle phase. Horm Behav 39:258–266. doi: 10.1006/hbeh.2001.1657 [DOI] [PubMed] [Google Scholar]
  35. Sigmon ST, Fink CM, Rohan KJ, Hotovy LA (1996) Anxiety sensitivity and menstrual cycle reactivity: psychophysiological and self-report differences. J Anxiety Disord 10:393–410. doi: 10.1016/0887-6185(96)00019-9 [DOI] [Google Scholar]
  36. Sigmon ST, Dorhofer DM, Rohan KJ, Boulard NE (2000a) The impact of anxiety sensitivity, bodily expectations, and cultural beliefs on menstrual symptom reporting: a test of the menstrual reactivity hypothesis. J Anxiety Disord 14:615–633. doi: 10.1016/S0887-6185(00)00054-2 [DOI] [PubMed] [Google Scholar]
  37. Sigmon ST, Dorhofer DM, Rohan KJ, Hotovy LA, Boulard NE, Fink CM (2000b) Psychophysiological, somatic, and affective changes across the menstrual cycle in women with panic disorder. J Consult Clin Psychol 68:425–431. doi: 10.1037/0022-006X.68.3.425 [DOI] [PubMed] [Google Scholar]
  38. Sigmon ST, Rohan KJ, Boulard NE, Dorhofer DM, Whitcomb SR (2000c) Menstrual reactivity: the role of gender-specificity, anxiety sensitivity, and somatic concerns in self-reported menstrual distress. Sex Roles 43:143–161. doi: 10.1023/A:1007036012911 [DOI] [Google Scholar]
  39. Smith H, Thomas SP (1996) Anger and locus of control in young women with and without premenstrual syndrome. Iss Ment Health Nurs 17:289–305 [DOI] [PubMed] [Google Scholar]
  40. Strine TW, Chapman DP, Ahluwalia IB (2005) Menstrual-related problems and psychological distress among women in the United States. J Womens Health 14:316–323. doi: 10.1089/jwh.2005.14.316 [DOI] [PubMed] [Google Scholar]
  41. Telch MJ, Silverman A, Schmidt NB (1996) Effects of anxiety sensitivity and perceived control on emotional responding to caffeine challenge. J Anxiety Disord 10:21–35. doi: 10.1016/0887-6185(95)00032-1 [DOI] [Google Scholar]
  42. White KS, Brown TA, Somers TJ, Barlow DH (2006) Avoidance behavior in panic disorder: the moderating influences of perceived control. Behav Res Ther 44:147–157. doi: 10.1016/j.brat.2005.07.009 [DOI] [PubMed] [Google Scholar]
  43. Yonkers KA, Pearlstein T, Rosenheck RA (2003) Premenstrual disorders: bridging research and clinical reality. Arch Wom Ment Health 6: 287–292. doi: 10.1007/s00737-003-0026-4 [DOI] [PubMed] [Google Scholar]
  44. Zebb BJ, Moore MC (1996) Another look at the psychometric properties of the anxiety control questionnaire. Behav Res Ther 37:1091–1103. doi: 10.1016/S0005-7967(98)00206-X [DOI] [PubMed] [Google Scholar]
  45. Zvolensky MJ, Lejuez CW, Eifert GE (1998) The role of offset control in anxious responding: an experimental test using repeated administrations of 20% carbon-dioxide-enriched air. Behav Ther 29:193–209. doi: 10.1016/S0005-7894(98)80002-6 [DOI] [Google Scholar]
  46. Zvolensky MJ, Eifert GE, Lejuez CW, McNeil DW (1999) The effects of offset control over 20% carbon-dioxide-enriched air on anxious responding. J Abnorm Psychol 108:624–632. doi: 10.1037/0021-843X.108.4.624 [DOI] [PubMed] [Google Scholar]
  47. Zvolensky MJ, Heffner M, Eifert GE, Spira AP, Feldner MT, Brown RA (2001) Incremental validity of perceived control dimensions in the differential prediction of interpretive biases for threat. J Psychopathol Behav 23:75–83. doi: 10.1023/A:1010935407194 [DOI] [Google Scholar]

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