Helping prostate cancer patients understand the causes of anxiety and depression: comparing cancer-caused vs patient response events

Original article

Helping prostate cancer patients understand the causes of anxiety and depression: comparing cancer-caused vs patient response events Keywords Prostate cancer Anxiety Depression Causes Counseling

Christopher F. Sharpley, PhD Centre for Bioactive Discovery in Health & Ageing, University of New England, New South Wales, Australia Vicki Bitsika, PhD Bond University, Gold Coast, Queensland, Australia David R.H. Christie, MB, ChB Premion, Queensland, Australia E-mail: csharpley@onthenet. com.au

Online 1 November 2009

Christopher F. Sharpley, Vicki Bitsika and David R.H. Christie Abstract Background: Prostate cancer (PCa) patients have elevated anxiety and depression, often showing impairments in decision-making and weakened relationships with their partner and family. Although treatment for these psychological side-effects of PCa is strongly recommended, relatively little is known of the causal processes underlying them. This study compared cancer-based lifestyle changes vs patient behavioural responses to cancer as predictors of anxiety and depression among PCa patients. Methods: PCa patients (381) were surveyed for their responses to standardised anxiety and depression questionnaires, plus a questionnaire designed to assess the kinds of lifestyle changes that had occurred to them and their responses to those changes. Results: Anxiety was most powerfully predicted by PCa-induced lifestyle changes but depression was most powerfully predicted by patient responses to those changes. Negative emotions, plus social withdrawal and worry were the underlying factors contributing most powerfully to combined anxiety–depression scores. Conclusion: PCa patient anxiety and depression may be instigated at different times and by different causal factors. In terms of possible treatment models, both supportive and action-based counselling strategies may be of benefit, but at different stages during the PCa patient’s experiences of diagnosis and treatment. ß 2009 WPMH GmbH. Published by Elsevier Ireland Ltd.

Introduction Prostate cancer (PCa) patients often have higher levels of clinical and subsyndromal anxiety and depression than their age-relevant peers [1–9], with up to 65% expressing a desire for assistance with these aspects of their disease [10] and 89% participating in therapy and education when available [11]. Unfortunately, psychosocial distress arising from cancer is often unrecognised [12], leaving many of these patients unidenti-

ß 2009 WPMH GmbH. Published by Elsevier Ireland Ltd.

fied and untreated, perhaps needlessly increasing the disease burden upon them, their family/ carers and the health system, as well as interfering with the effectiveness of their treatment decisions [13]. Thus, early identification and treatment of anxiety and depression among PCa patients remains of critical importance [14]. When stressful events occur, such as receiving a diagnosis of PCa, individuals respond in various ways. Coupled with genetic predisposition, individuals’ responses to stressful events

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Original article may later lead to the development of anxiety [15] and depression via the ‘‘diasthesis-stress hypothesis of mood disorders’’[16]. For example, some patients may develop symptoms such as crying, fatigue, sleeping difficulties, digestive problems, elevated heart rate, restlessness, muscle tension, sweating and trembling, changes in appetite and weight and loss of energy. All of these are diagnostic criteria for anxiety and/or depression [17], two disorders which may be related by exaggerated activity of the hypothalamic–pituitary axis [15,18,19]. Persons suffering from anxiety and depression may also show pathological worry, prolonged arousal, lowered immune functioning, fatigue, low-level infections and feelings of helplessness and pessimism that the future will offer any respite, leading some to claim that these two disorders are interrelated in symptomatology [17] and nature [20], a relationship that has been recognised by the diagnostic classification of ‘‘mixed anxiety/ depression’’ [21]. Thus, it could be argued that anxiety and depression may be linked within the symptomatology of some individuals, and that therefore assessment and treatment of both anxiety and depression in tandem, rather than separately, is recommended. Although the presence of symptoms of anxiety and depression may be assessed via clinical interview [17] or via a range of standardised diagnostic tests, these procedures measure the presence of the clinical symptoms of anxiety and depression but do not necessarily evaluate the events or issues which caused the anxious or depressive symptomatology or the individual’s behavioural (i.e. coping) responses to the event and/or the presence of symptoms of anxiety or depression. Although some of these coping responses may later constitute the diagnostic criteria for anxiety and depression, they are not always synonymous with those criteria. For example, the death of a loved one (the stressful event) may initiate sadness, loss of pleasure in activities and sleep disturbances (all of which constitute criteria for depression [17]), but the associated and particular behavioural (coping) responses of the depressed individual (such as refusal to attend social occasions, reducing playing of a particular sport or engaging in a specific recreational activity) are not specifically assessed or identified by the diagnostic criteria per se. However, accurate identification of the particular stressful event experienced by PCa

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patients, plus their behavioural (coping) responses to that event can be productive targets for individual therapy and behaviourchange strategies with cancer patients [22,23], and a recent review indicated that this kind of specifically targeted therapy was more successful with cancer patients’ psychological distress than generalised treatments [24]. Certainly, receiving a diagnosis of PCa and treatment are major life stressors which may lead to the symptoms described above and the consequent decreased cognitive functioning and lowered mood that are found in anxiety and depression. There are many aspects of that diagnosis and its treatment (e.g. issues of mortality, fatigue from the PCa itself, anxiety regarding loved ones, nausea, pain) which may constitute the specific cancer-based stressor that initiates anxiety and depressive symptomatology within particular PCA patients. Similarly, patients may vary in the ways they seek to cope with those stressors via their own behavioural responses to the specific aspects of the cancer diagnosis and treatment. Therefore, treatments targeting the events and changes that PCa patients experience as a result of their disease, plus their responses to those changes, may fit into the kinds of interventions which have been shown to be most effective in alleviating the distress of PCa patients. However, prior to those treatments, the particular kinds of cancer-caused stressors experienced by PCa patients that contribute to the development of anxiety and depression need to be reliably identified. In addition, the specific ways in which PCa patients cope via their behavioural responses also need to be identified. Therefore, this study aimed to extend two previous studies conducted into PCa patients’ experiences [25,26] by comparing the relative strength of (1) the stressor events and changes undergone by PCa patients as a result of their disease or its treatment and (2) patients’ behavioural responses to those disease-based events or changes, as predictors of anxiety and depression.

Methods Participants A total of 341 PCa patients living in Brisbane, Australia participated in a mailout survey. Ages of participants ranged from 52 years to

Original article 87 years (M = 67.02 years). Their mean time since diagnosis was 13.9 months, ranging from 1 to 96 months. All participants had cancers limited to the primary site and regional draining lymph nodes using conventional staging investigations. In terms of their present disease status, most (70.1%) reported that their cancer was still present and that they were receiving initial treatment, 24.6% were in remission and 5.4% were receiving additional treatment for recurring cancer. Current treatment varied, with 24.6% receiving radiation therapy, 2.4% undergoing surgery and 38.9% receiving antiandrogen hormone treatment, while 37.8% reported that they were currently receiving no treatment.

Materials and Materials Background questionnaire Age, living situation, month and year of first diagnosis, present status of their cancer. Zung Self-Rating Anxiety Scale (SAS) [27] The 20-item SAS is based on DSM [17] definitions of anxiety and drawn from ‘‘the most commonly found characteristics of an anxiety disorder’’ [27: 371]. Positively- and negativelyworded items reduce response bias and reversed items act as a lie scale. Respondents are asked to indicate how they have felt during the last week according to: ‘‘None or a little of the time’’ (scored as 1), ‘‘Some of the time’’ (2), ‘‘Most of the time’’ (3) or ‘‘All of the time’’ (4). Total raw scores range from 20 to 80, with higher scores indicative of greater anxiety. The SAS correlates 0.75 with the Hamilton Anxiety Scale [27] and significantly discriminates between normal adults and patients with anxiety disorders [27]. Reliability data are 0.71 (split half: [27]) and 0.79 (coefficient alpha) in an Australian sample of 552 non-cancer participants [28] and between 0.74 and 0.77 for two samples of Australian PCa patients (n = 195, 150, respectively) [26,29]. Zung stated that raw scores above 36 indicated that participants had ‘‘clinically significant’’ anxiety [30: 18]. Zung Self-Rating Depression Scale (SDS) [31] The SDS has 20 items that were identified in factor analytical studies of the syndrome of depression and which underlie the DSM definition [17] and is set out in the same format as

the SAS. The SDS has a split-half reliability of 0.81 [31], 0.79 [32] and 0.94 [33]. Internal consistency (alpha) has been reported as 0.88 for depressed patients and 0.93 for non-depressed patients [32], and as 0.84 and 0.83 for previous Australian PCa samples [26,29]. The SDS has been shown to be superior to the MMPI Depression Scale and the Beck Depression Inventory for assessing depression in male psychiatric inpatients [34]. Zung recommended a cutoff score of 40, above which respondents could be described as having ‘‘clinically significant depression’’ [31: 335]. SDS and SAS raw scores were used in this study. The Effects of Prostate Cancer on Lifestyle Questionnaire (EPCLQ) This is a 36-item measure developed from 50 events identified by PCa participants in a replicated individual interview study as causing them major psychological distress [25] and later refined to 36 items [26]. Participants in the current study were invited to complete this latter version of the EPCLQ using the same four-point scale as for the SAS and SDS. Total scores ranged from 36 to 144. Methods In total, 800 PCa patients were mailed a letter inviting them to participate in the survey and 341 (42.65%) returned usable questionnaires. All responses were coded so that participants were anonymous. All procedures were approved by the Uniting Health Care Human Research Ethics Committee.

Results The mean and range of age of these participants was not dissimilar to other samples of PCa patients from this general geographical area [25,26] and there were no significant differences in SAS or SDS scores according to present cancer status or according to their current treatment. Reliability (Cronbach’s alpha) was satisfactory for the SAS (0.78), SDS (0.84) and the EPCLQ (0.88), justifying further examination of the data from these scales [35]. The mean SAS score was 32.23 (standard deviation (SD) = 6.93), median = 32.23, with a range of from 20 to 64/80. The 5% trimmed mean was 31.93, only 0.30 below the sample mean, indicating negligible

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Original article effects on the mean score from outliers in the sample. Evaluation of skewness and kurtosis (measures of the symmetry and peakedness of the distribution) showed that these SAS data may be accepted as meeting the requirements of normality. Using Zung’s cut-off score of 36, 90 (23.9%) of the sample were experiencing ‘‘clinically significant’’ anxiety [30]. The mean SDS score was 34.08 (SD = 8.831), median = 34.0, range from 20 to 66/80. The 5% trimmed mean was 34.68, only 0.60 greater than the sample mean and allowing outlier effects to be discounted. Skewness and kurtosis were acceptable. Using Zung’s cut-off score of 40, 98 (26.0%) of the sample were clinically depressed [31]. The incidence of clinically significant anxiety and depression among this sample was within the overall range from the wider literature on PCa patients [9]. The mean total score for the EPCLQ was 65.69 (SD = 13.12), median = 63.5, range from 38–134 from a possible range of 34 to 144. The 5% trimmed mean was 64.76, only 0.92 less than the sample mean, indicating that outlier effects were minimal. Skewness and kurtosis were again acceptable. In order to categorise the EPCLQ items into (1) those items which described the direct stressors arising from PCa (‘‘Cancer-caused’’) and (2) items which represented patients’ behavioural (coping) responses to those stressors (‘‘Behavioural responses’’), each of the first two authors blindly identified all EPCLQ items according to the definitions: ‘‘Events and PCarelated changes to patients over which they had no control, e.g. pain, nausea, fatigue, decreased memory ability’’ (Cancer-caused: n = 15) and ‘‘Patient responses to PCa and PCa-related changes, including only those behavioural responses over which they could have exerted some control, e.g. playing sports with others less, not getting on so well with wife or partner’’ (Behavioural responses: n = 21). These categories and the items that were chosen to fit them were later confirmed by a panel of three experienced psychologists, each of whom was also blind to the other two panel members’ evaluations of the two EPCLQ subscales developed using the above procedure. To investigate the relative power of the two subscales of EPCLQ items in predicting anxiety or depression, regression analysis was performed using total SAS and SDS scores as the dependant variable, each in a separate regres-

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sion analysis, and the two EPCLQ subscales as the predictor variables. When compared as predictors for SAS scores (R square = 0.404 (F(2, 370) = 124.806, P < 0.001) (R square indicates the amount of variance in the dependent variable that is explained by the regression model used), Cancer-caused events were more powerful in predicting SAS scores (b = 0.387, t = 7.419, P < 0.001) than Behavioural responses (b = 0.316, t = 6.054, P < 0.001). Because the b values for both predictor variables were similar, several further analyses were conducted to determine the relative contribution of each to SAS score. First, the 95% confidence intervals (CI) were noted as not overlapping (Cancer-caused = 0.335–0.577; Behavioural responses = 0.166–0.325); second, the t-tests for each predictor variable were significant, indicating that each was making a statistically significant unique contribution to the regression equation [36]; and third, by examining the part correlations (i.e. the semipartial correlation coefficients [37]) which indicate the unique contribution of each predictor variable to SAS score over and above the other predictor variable [38], the percentages of the total variance of SAS score uniquely explained by Cancer-caused (8.9%) and Behavioural responses (5.9%) were determined. These extra analyses indicated that, when examined independently of each other, the relative unique contribution of Cancer-caused items to SAS score was significantly and meaningfully greater than that made by Behavioural response items in the EPCLQ. For SDS scores, R square was 0.373 (F = 109.467, P < 0.001) and the b weights showed that, although both variables significantly contributed to SDS total score, Behavioural responses (b = 0.387, t = 7.236, P < 0.001) were more powerful than Cancer-caused events (b = 0.287, t = 5.366, P <0.001). Again, examination of the significance levels of the t-tests and the part correlations showed that the apparent relative strength of Behavioural responses over Cancer-caused events in predicting SDS scores was supported by these statistics. Assumptions were satisfied in both regressions. Logistic regression was used to explore the relative power of the two EPCLQ subscales in predicting clinical anxiety or depression, using the same EPCLQ subscales as independent variables and SAS or SDS clinicity (i.e. whether patients had SAS or SDS scores that were above the cutoff levels stipulated by Zung

Original article [29,30]) as the dependant variables. For SAS, the two EPCLQ subscales produced a statistically significant model (x2 (2) = 75.094, P < 0.001) and the model correctly classified 79.0% of the cases, with the Cancer-caused subset of EPCLQ items having a higher significant Wald test value (17.130, P < 0.001) than the Behavioural responses (11.256, P < 0.005). For the SDS data, the model was also significant (x2 (2) = 81.314, P < 0.001) and correctly classified 79.7% of the cases. Behavioural responses (Wald Test = 24.312, P < 0.001) were more powerful predictors of SDS clinicity than Cancer-caused events (Wald Test = 6.917, P < 0.005). To determine which of the items in the two EPCLQ subscales were most strongly associated with overall anxiety and depression, Multivariate Analysis of Variance was performed on the items in each of the EPCLQ subscales separately, using SAS and SDS ‘‘clinicity’’ categories as the dependent variables. There were significant main effects for SAS and SDS but not for the interaction of SAS and SDS. Table 1 shows the EPCLQ subscale items ranked according to the strength of their particular F value across anxiety and depression clinicity (P< 0.002, based upon a Bonferroni correction (a correction to set all alpha levels across tests at equal sizes) for the number of items in each subscale). Mean values for clinically significant patients were greater than for those patients whose SAS/SDS scores did not reach Zung’s cutoff levels for clinically significant anxiety or depression. From Table 1, it is apparent that there was considerable overlap in the EPCLQ items which

discriminated between clinically significant anxiety and clinically significant depression, which may be due to the common symptomatology between these two disorders [20,21]. Further regression analyses of the two EPCLQ subscales against the combined SAS and SDS scores confirmed the previous findings by showing that the combined anxiety–depression scores were predicted by Behavioural responses (b= 0.379, P < 0.001) and Cancercaused antecedents (b = 0.348, P < 0.001). As a final step in determining the nature of the two EPCLQ subscales, Factor Analysis was performed on each of them and the factors were then entered into regression analyses with the combined SAS–SDS scale as the dependent variable. For the Cancer-caused EPCLQ subscale, two components had eigenvalues (a measure of the total variance explained by a particular factor) greater than 1.0, supported by the scree plot and parallel analysis, with the two factors accounting for 41.61% of the variance. Using a forced analysis via Oblimin rotation (to present a pattern of loadings that is easier to interpret), 12 of the 16 EPCLQ items loaded on to one or the other of these two factors. Examination of the first factor (29.55% of the variance) showed six EPCLQ items loading on to it, including: being tired, decreases in memory ability, alertness and concentration, being ‘‘fuzzy’’ about organising things and feeling worse overall, suggesting that this factor might be defined as ‘‘Cognitive deficits’’. Factor 2 (12.06% of the variance) included the items: poorer sleeping, difficulties

Table 1 EPCLQ subscale items from MANOVA ranked in size of univariate effect for anxiety and depression clinicity (all P < 0.002) Cancer-caused

Behavioural responses

Anxiety

Depression

Anxiety

Depression

Tired Nauseous

Tired ‘‘Fuzzy’’ about organisation Reduced concentration Feeling worse overall

Feeling depressed More anxious

Disappointed Sadder

Angry

Depressed

Less tolerant of others Withdrawing from others

More anxious

Decreased memory ability Feeling worse overall Increased pain Poorer sleeping ‘‘Fuzzy’’ about organisation

Angry Withdrawing from others Getting on worse with friends Less tolerant of others

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Original article in passing urine and bowel motions, increased need for bowel motions, and increased pain and nausea, allowing this factor to be termed ‘‘Physiological problems’’. These two factors were entered into a regression analysis with the combined SAS–SDS total score as the dependent variable. R-square was 0.412 (P <0.001). Factor 1 was the strongest predictor of SAS–SDS scores (b = 0.474, t = 10.666, P < 0.001), followed by Factor 2 (b = 0.273, t = 6.140, P < 0.001). For patient Behavioural responses, examination of the scree plot and parallel analysis indicated a four-factor solution, which accounted for 58.39% of the variance. Using a forced analysis via Oblimin rotation, all 21 EPCLQ items loaded on to one or the other of these four factors. Factor 1 (27.76% of the variance) had EPCLQ items including: being tired, and feeling depressed, anxious, angry, disappointed and sadder, suggesting that it might be defined as ‘‘Negative emotional responses’’. Factor 2 (15.26% of the variance) included the items: decreased exercise, including running, walking, cycling, swimming, playing bowls or golf and fishing or boating, allowing this factor to be termed as ‘‘Reductions in sport and exercise’’. Factor 3 included items concerned with: loss of professional or trade identity and fulltime work and income, which was identified as ‘‘Employment withdrawal’’. Factor 4 loaded on to items concerned with: decreases in work or hobby productivity, reduced sporting activities with others, not getting on well with friends, and feeling more worried about the future, and this factor was called ‘‘Social withdrawal and worry’’. These four factors were entered into a regression analysis with the combined SAS–SDS total score as the dependent variable. The Rsquare was 0.506 (P < 0.001). Factor 1 was the strongest predictor of SAS–SDS scores (b = 0.570, t = 13.865, P < 0.001), followed by Factor 4 (b = 0.267, t = 7.134, P < 0.001) and neither of the two remaining factors were significant predictors of SAS–SDS combined scores.

Discussion This exploration of the comparative power of cancer-based events/changes and patientinitiated behavioural responses to those events/changes indicated that anxiety was most powerfully predicted by disease-based

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changes to patients’ physical abilities, such as poorer sleeping, difficulties passing urine and bowel motions and nausea and pain. A second, slightly less powerful predictor of anxiety was the behaviours that PCa patients engaged in as a result of their cancer, such as withdrawing from others, feeling angry, anxious and disappointed, and decreasing sporting activities. Although causality in this equation connecting PCa-caused physical changes and patient responses to those changes with anxiety is by no means clearcut and may be influenced by other patientcentred variables, the overall finding described above allows anxiety to be conceptualised as a group of physiological arousal responses normally engendered when the organism is threatened or in pain. It is quite conceivable that these PCa patients were frightened about their future when they received their diagnosis, and that their responses were exacerbated by the onset of physical disease-caused symptoms such as those described in the Cancer-caused subscale. The same predictor pattern was apparent when patients were allocated into categories on the basis of having experienced clinically significant anxiety or not. By contrast, depression was most powerfully predicted by patients’ behavioural responses, and then by cancer-caused physical changes. This juxtaposition of the two EPCLQ subscales suggests a theoretical model in which anxiety and depression may be stages along a continuum of physiological arousal to a major threat which could not be removed. That is, the first stage of responsivity to PCa-based changes in physical functioning was those anxiety responses which are designed to help the organism escape or avoid threat (e.g. increased heart rate and blood pressure, sweating, slowdown of digestion, muscle agitation and trembling). When these autonomic escape responses did not help patients avoid the diagnosis, its treatment and ensuing physical changes, then patients reacted with a range of behavioural responses which were characterised by the withdrawal mechanisms previously shown to underlie depression [39]. The same predictor pattern was shown when patients were divided into those with clinically significant depression and those without. Examination of the relative power of the items in the EPCLQ subscales showed several communalities across anxiety and depression.

Original article For example, fatigue, feeling worse overall and being ‘‘fuzzy’’ about organisational tasks were significantly associated with both anxiety and depression clinicity in the Cancer-caused subscale. Similarly, feeling depressed, angry, more anxious and less tolerant of others, plus actively withdrawing from others, were all common items from the Behavioural responses subscale for anxiety and depression. These data reinforce the commonalities between anxiety and depression that were mentioned in the Introduction, above. Regression of the two EPCLQ subscales against the combined SAS–SDS scores lent support to this communality. When examined for their underlying factors and the predictive power of those factors for anxiety and depression, Cancer-caused ‘‘Cognitive deficits’’ were stronger than Cancercaused ‘‘Physiological problems’’, suggesting that decreases in memory, alertness, concentration and organisational ability were more likely to lead to elevated anxiety–depression scores than problems in sleeping, urination and bowel motion difficulties, and pain and nausea. Four factors were extracted from the EPCLQ subscale Behavioural responses, but only two of these significantly predicted SAS–SDS scores. ‘‘Negative emotions’’ were the most powerful predictor of anxiety–depression, with ‘‘Social withdrawal and worry’’ predicting SAS– SDS scores at a much less powerful level. Although most studies of anxiety and depression among PCa patients assess the presence and severity of these disorders via standardised tests (as in the present study), note should be taken of the potential for discrepancy between that kind of data and the presence of actual ‘‘clinical’’ diagnoses of anxiety and depression against the common yardstick of the DSM-IV-TR [17]. That is, correlational studies may correctly show relationships between various factors and anxiety/depression scores, but these do not necessarily imply that the sample was clinically anxious or depressed. In fact, receiving a diagnosis of, and treatment for, PCa would be a predictable stressor which could induce anxiety and depression at higher than usual levels. However, two caveats should be kept in mind when dealing with the kinds of elevated anxiety and depression scores which were found in the present sample lest they be discarded as not of clinical significance. First, even those

patients whose anxiety or depression symptomatology does not meet formal DSM-IV-TR criteria for a Depressive Disorder may fulfill the criteria for subsyndromal anxiety or depression (i.e. less than the required number of symptoms present), and there are well-established data which show that patients with subsyndromal anxiety and depression experience the same kinds of psychosocial impairment as patients who meet the criteria for Major Depressive Disorder [40] including increased risk of developing Major Depression and suicide [41], leading to the comment that ‘‘subsyndromal depression (is) a matter for serious consideration by clinicians and researchers’’ [42: 38]. Second, and as mentioned in the Introduction, above, as a group, PCa patients have higher levels of clinical and subsyndromal anxiety and depression than their age-relevant peers [1–9]. In addition, nearly two-thirds of the samples from previous studies expressed a desire for assistance with their feelings of anxiety and depression [10], and 89% took part in therapy and education when it was offered to them [11]. Thus, even though caution should be used when examining anxiety and depression data from PCa samples such as the one used in this study, the implications of even moderately elevated anxiety and depression for PCa patients’ daily lives, plus their expressed desire for assistance with these aspects of their illness, argue for the serious consideration of anxiety and depression data collected in studies such as this one. Limitations of this study include generalisability from the sample (size, demographic qualities); the EPCLQ items from which the two subscales were drawn which were developed on a similar demographic sample as that used in this study; the collection of data at one particular time during the patients’ illness and treatment, with no measure of variability over time; and the relatively small number of patients receiving surgery for their PCa, which may have biased the sample towards radiotherapy patients and their PCa-related stressors and behavioural responses. However, while bearing these limitations in mind, some suggestions may be made for the use of these data within treatment regimes for PCa patients. Although the kinds of physiological and psychological sequelae of receiving a diagnosis of, and treatment for, PCa are challenging and may sometimes simply have to be

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Original article endured, the exaggerating of normal physiological arousal as an escape response to threat, plus intensifying of the longer-term and potentially more distressing withdrawal responses that characterise depression, may be the results of different causal processes. By demarking those possible causes into cancerbased versus patient responses, anxiety and depression become more amenable to focused counselling interventions, which are more likely to be successful than generalised therapy approaches [23]. For example, in those cases where the causal agent for patient anxiety or depression is mostly associated with PCa-based events, supportive counselling, perhaps following a Client-centred model [43], could be used to assist the PCa patient through what are unavoidable aversive side effects of the disease

or its treatment. That support could also assist patients in addressing their concerns regarding pain management, duration of discomfort and lifetime of those effects to their oncologist. By contrast, when symptoms of anxiety or depression are an outcome of the patient’s own behavioural responses to the PCa-based changes, then intervention might take a more solution-focused role, applying cognitive and behaviour therapy approaches [41,44] designed to assist the patient to clarify responses to the PCa and understand the impact of these responses on daily functioning. This intervention would also assist the patient to adopt alternative positive responses to PCa and build coping skills to handle aversive events such as PCa-induced pain and discomfort.

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