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Psychosomatic Medicine 68:734-741 (2006)
© 2006 American Psychosomatic Society

ORIGINAL ARTICLES

Effects of Naltrexone on Repressive Coping and Disclosure of Emotional Material: A Test of the Opioid-Peptide Hypothesis of Repression and Hypertension

Jarred W. Younger, PhD, Kathleen A. Lawler-Row, PhD, Krista A. Moe, BS, Anna L. Kratz, MA and Amy J. Keenum, DO, PharmD

From the Division of Pain Management, Department of Anesthesia, Stanford University School of Medicine, Palo Alto, California (J.W.Y.); the Department of Psychology, University of Tennessee, Knoxville, Tennessee (K.A.L.-R.); the Department of Educational and Counseling Psychology, University of Kentucky, Lexington, Kentucky (K.A.M.); the Department of Psychology, Arizona State University, Tempe, Arizona (A.L.K.); and the Department of Family Medicine, University of Tennessee Graduate School of Medicine, Knoxville, Tennessee (A.J.K.).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 MATERIALS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: The present study was designed to assess the role of endogenous opioids in the relationship of hypertension to repressive coping.

Methods: Ten hypertensive and 8 normotensive males were given either the opioid antagonist naltrexone or placebo in a randomized, double-blind fashion over the course of four laboratory sessions. Measures of repression and disclosure were completed and blood pressure was assessed during a laboratory stressor protocol.

Results: Opioid antagonism reduced repression and increased disclosure only in the hypertensive group. Also, opioid antagonism increased stress-related systolic blood pressure only in the hypertensive group.

Conclusion: The results support the hypothesis that endogenous opioid dysregulation underlies both hypertension and repressive phenomena.

Key Words: hypertension • repression • disclosure • opioids • comorbidity • naltrexone

Abbreviations: DBP = diastolic blood pressure; SBP = systolic blood pressure; POMS = Profile of Mood States; LCC = Life Concerns Checklist; MAS = Taylor Manifest Anxiety Scale; MCSDS = Social Desirability Scale; TAS = Toronto Alexithymia Scale.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 MATERIALS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Under the new guidelines set forth by the Joint National Committee (JNC) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, an estimated 60% of American adults are hypertensive or prehypertensive (1). Hypertension, a leading cause of stroke, myocardial infarction, and heart failure (2), is one of the most dangerous conditions in the industrialized world. Although risk factors such as obesity and family history have been identified (3,4), the etiology of hypertension is largely unknown. One intriguing relation, with possible causal properties, exists between hypertension and psychological repression. Individuals who exhibit chronically or acutely elevated levels of blood pressure are more likely to manifest signs of repression, as evidenced by diminished reporting of stress, negative affect, and pain (5–18).

Although repression has proven to be a difficult concept to assess (19), it can be defined as motivated nonretrieval of anxiety-producing material (20,21). Repression has been further described as an unconscious process by which threatening events or states are kept out of conscious awareness (22). This definition is in contrast to suppression, in which avoidance is conscious (23). Based on this delineation, suppression involves the inward experience of negative affect with inhibited behavioral expression, whereas repression involves no conscious experience of negative affect (24). Although the distinction between these concepts is debatable (25), the two have been distinguished experimentally in the laboratory (26). Both suppression and repression have been linked to cardiovascular problems (27,28), although the respective mechanisms may be different. The present report deals exclusively with the concept of repression while acknowledging the interchangeable way in which these two concepts are sometimes used in the literature.

The relation between hypertension and repression has been identified in a number of correlational and quasiexperimental studies. Blood pressure is inversely correlated with self-reported stress (7–10). Also, those with hypertension or elevated blood pressure report fewer personal concerns (5,6) and significant life events (11,12) than normotensives. This attenuated reporting of stress extends to self-reported neurotic symptoms (13) as well as cold pressor (14), finger pressure (15), thermal (16), and electrical (17) pain. The diminished reporting of hypertensives generalizes to both physical and psychological stressors (18).

The results of these studies are most striking in how they differ from the large body of evidence suggesting a positive relation between stress and blood pressure in the general population (29–32). A meta-analytic review of psychosocial stressors and hypertension or elevated blood pressure concluded that the direction of the relationship depended on whether objective or subjective measures of stress were used (33). When objective measures were used, a strong positive correlation between stress and blood pressure was observed. This relationship, however, was nonexistent or even inverted when self-report scales were used as a measure of stress. An altered basis of stress appraisal in comorbid hypertension and repression subgroups (10,33,34) may explain this discrepancy.

One of the more recent tools for assessing repression involves crossing scores of individuals on anxiety and defensiveness questionnaires (35). The "repressive coping style" is identified by low scores of state anxiety (measured, for example, by the Taylor Manifest Anxiety Scale (36)) with high scores of defensiveness as measured by the Marlowe-Crowne Scale of Social Desirability (37). This index is proposed to reflect a tendency to underreport negative experiences. Repressive copers exhibit greater physiological stress responses than either highly anxious or low anxious groups (38), a finding that has been supported by meta-analysis (39). Taken together, these findings suggest a robust relationship between repression and hypertension with increased blood pressure (both chronic and acute) being associated with diminished self-reports of stress, pain, neurotic symptoms and negative affect.

Although the correlational relation between hypertension and repression is well established, the issue of directionality is less clear. Most theoretical writing on the subject focuses on how repression might cause hypertension. These hypotheses range from Freudian hydraulic (40) and cathartic (41,42) models to more contemporary sympathetic system demand models (43,44). Evidence for these claims is limited, however, and comes mostly from case studies in which a reduction of blood pressure is observed after disclosure of a traumatic event (45). Because the frequencies of cardiovascular measurements are low (e.g., weekly), it is impossible to determine whether disclosure precipitated the blood pressure drop or the converse. The benefits of disclosure have also been studied in the laboratory (46); however, results are difficult to interpret because disclosure was an unassigned variable and blood pressure recovery was similar for both traumatic and mundane event disclosure.

A larger, albeit quieter, literature indirectly supports the hypothesis that hypertension may lead to repressive phenomena. Early hypotheses posited that repression was a dependent effect of sympathetic activity on the brain (47). Although no work has experimentally tested hypertension’s effect on repression, much has been done on hypertension and pain. Pain may be seen as a reasonable analog of negative affect because both phenomena involve states resulting from noxious stimuli and because repressive copers respond to both in a diminished fashion. It is possible, then, that the two phenomena share similar physiological mechanisms. Evaluating pain and hypertension relationships allows animal studies to be conducted in which blood pressure manipulation would be impractical in humans. Indeed, experimental increases of blood pressure in rats, induced either by injection of adrenergic agonists (48) or by clip on the renal artery (49), increase pain tolerance.

Experimental evidence has identified a plausible mechanism by which heightened blood pressure levels may cause antinociception. In the Dworkin et al. (48) study, elevated blood pressure reduced escape–avoidance behavior but did not reduce that behavior in rats with surgically denervated baroreceptors (receptors designed to detect and maintain blood pressure levels). Furthermore, direct stimulation of baroreceptors has been found to produce the same behavioral results as increased blood pressure (50,51). Therefore, blood pressure may operate through the activation of baroreceptors to reduce noxiousness (16).

Research with naloxone, an opioid antagonist, has further suggested that baroreceptors may play a role in antinociception through their effect on endogenous opioid systems. Saavedra (52) found that although naloxone negated the increased pain tolerance exhibited by hypertensive rats, it had no effect on normotensive rats. Similar results have been found with stress-induced blood pressure increases in humans (53).

Although baroreceptors reduce blood pressure through innervation of the medulla oblongata, limbic and neocortical influences on sympathetic activity (i.e., the conscious experience of threat) may necessitate additional, indirect paths for regulating the sympathetic response. High concentrations of mu-opioid receptors in the amygdala, hippocampus, cingulate cortex, and other limbic structures suggest that endogenous opioids, through their effects on affective systems, diminish the stress response (54,55). Similar to the effect of exogenous opiates, endogenous opioid activity would likely result in less experience of stress, pain, and threat. These experiences, coupled with high blood pressure, are characteristic of repressive copers in the laboratory. The repressive coping style may result from blood pressure-induced, baroreceptor-mediated endogenous activity.

The role of endogenous opioids in repression has not been specifically tested. The present study extends previous work on hypertension and pain to include negative psychological states. Specifically, the role of endogenous opioids in comorbid hypertension and repression cases is examined. In the present study, normotensives and hypertensives participated in four laboratory sessions in which they disclosed concerns, stressors, and mood and completed measures of repressive coping and disclosure. In two of the sessions, individuals were administered naltrexone, an opioid antagonist. In the other two sessions, a placebo was administered. Administration was double-blind and the schedule was randomized. It was hypothesized that naltrexone would increase disclosure and decrease repressive coping in hypertensives (HTs) but not in normotensives (NTs).


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
MATERIALS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participants
Male undergraduate students were solicited through extra credit announcements from the Department of Psychology at the University of Tennessee. Volunteers (n = 125) were invited to participate in a short cardiovascular and medical screening procedure for nominal extra credit in a psychology course. Recruitment, consent, and study procedures were approved by the University of Tennessee, Knoxville Institutional Review Board and the study was conducted in Spring of 2003. Blood pressure readings were taken with a Critikon Dinamap 1846 Vital Signs Monitor at 2-minute intervals for a 15-minute period. Resting levels were calculated by averaging the last three readings. Individuals who completed the initial cardiovascular screening were allowed to continue in the experiment if their systolic blood pressure fell in the upper or lower deciles of the sample distribution. Volunteers also completed a medical history questionnaire, which screened for secondary causes of hypertension (e.g., diabetes and kidney problems) and conditions in which naltrexone is contraindicated (e.g., alcoholism, narcotic abuse, narcotic medicine use, hepatitis, and clinical depression).

Twelve hypertensives and 12 normotensives were selected into HT or NT groups and all individuals accepted the invitation for further participation. Of these individuals, two withdrew the day of their first session. One individual’s participation was terminated after a missed first session and difficulty regaining contact. One participant from the HT group withdrew from the study citing adverse events from the drug administration, including agitation and fatigue. The remaining sample ranged in age from 18 to 25 years (mean, 20.28 years). The participants consisted of 17 whites and 2 blacks. Mean blood pressure for the NT group was 101/55 mm Hg (standard deviation (SD) = 4.6/4.2) with a range of 94 to 108 mm Hg systolic and 49 to 59 mm Hg diastolic. The HT group had a mean blood pressure of 139/65 mm Hg (SD = 4.2/6.5) with a range of 132 to 145 mm Hg systolic and 52 to 74 mm Hg diastolic. Five individuals in the HT group met prehypertensive criteria (>120 mm Hg systolic blood pressure (SBP) or >80 mm Hg SBP) and five met hypertensive criteria (>140 mm Hg SBP or >90 mm Hg diastolic blood pressure). Groups did not differ on age (t (16) = –0.5; p = .617). No participants were on antihypertensive medications. Groups differed on body mass index (BMI) (t (16) = –3.68; p = .002) with the HT group showing significantly greater BMI than the normotensive group. Although no between-groups analyses were performed, BMI was tested as a covariate in all analyses involving cardiovascular-dependent measures. When BMI did not enter the model as a significant covariate, final results are presented without controlling for BMI.

Measures
To investigate possible mood effects of naltrexone, an abbreviated version of the Profile of Mood States (POMS (57)) was used. The POMS measures anger, depression, anxiety, vigor, fatigue, and confusion using a Likert-type, 5-point scale. Subscales of the abbreviated version yield alphas from 0.66 to 0.95 with a mean of 0.80 indicating good internal consistency.

Disclosure was measured by the Life Concerns Checklist (LCC (58)). The LCC contains 34 areas about which a person may be concerned in his or her life. The scale has good test–retest reliability over 5 weeks (r = 0.85, p < .01). Internal reliability, measured with the Kuder-Richardson formula for scales with unidimensional constructs, was high (rKK = 0.93).

Repressive coping was measured by the Index of Self-Regulation of Emotion (ISE (59)), which creates a continuous measure of repression by crossing the Taylor Manifest Anxiety Scale, Bendig Short Form (MAS (60)) and the Social Desirability Scale (MCSDS (38)). The ISE’s continuous measurement of repression is ideal for measuring change resulting from a drug intervention. The MAS is a scale of state anxiety, whereas the MCSDS is a popular scale of defensiveness.

Alexithymia is a condition that has superficial similarities to repressive coping but is hypothesized to have a distinct etiology (61,62). Effects of naltrexone on alexithymia were measured using the Toronto Alexithymia Scale, 20-item version (TAS (63)). This version of the TAS has been found to have high internal consistency ({alpha} = 0.85)


   MATERIALS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 MATERIALS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Experimental manipulation of opioid activity was achieved with the opioid antagonist naltrexone (64). Naltrexone effectively blocks activity at mu-opioid receptors (65). It is orally administered, reaches peak absorption levels in an hour, and has a half-life of approximately 4 hours (66). In healthy volunteers, naltrexone has not been shown to present any significant adverse effects (67). Revia brand naltrexone is administered as a 50-mg tablet. For the present experiment, these tablets were inserted into a green opaque gelcap to maintain similarity in appearance with the placebo. An equal amount of nonactive substance (sugar pill) was placed in a gelcap to serve as the placebo.

Procedures
Participants were asked to schedule four laboratory visits over a 2-week period with each visit lasting approximately 1 hour 45 minutes. On arrival, participants were administered either naltrexone or placebo in a double-blind, randomized fashion. Each participant was given the active drug on two occasions and the placebo on two occasions. After drug or placebo administration, participants were seated and their cardiovascular group status (high or low) reconfirmed. Next, participants waited 1 hour to allow for peak absorption of the drug. During this time, participants were allowed to bring their own work or they could choose from television programs, video games, or magazines that had been screened to ensure the absence of strong emotional content. After the 1-hour absorption period, blood pressure was assessed with three readings taken at 2-minute intervals. These three readings served as the physiological baseline.

After baseline cardiovascular measurements, participants completed the interview stage. These interviews were audiotaped for later transcription and analysis. Blood pressure measurements continued at 2-minute intervals throughout the duration of the interview. Blood pressure was averaged over either two or three measurement periods, depending on the length of the interview. Participants were asked three questions and were told to think about each question for 30 seconds before responding. Participants were allowed to answer each question without time constraints or interruption. No follow-up questions were asked. First, participants were asked to talk about whatever came to mind. Second, they were asked to talk about the last 24 hours. Third, they were asked to talk about whatever situation was currently causing them the most stress or anxiety.

After the interview, participants filled out the scales of mood, repression, and disclosure: POMS, MAS, LCC, TAS, and MCSDS. The order of the measures was counterbalanced across sessions. Two additional blood pressure measurements were taken with a 2-minute interval during this period to serve as a pseudorecovery period.

Given the complex nature of any cognitive or affective system, we tested for delayed effects of naltrexone on disclosure. Participants completed diaries before going to bed each day of a laboratory session. Each participant was given a notebook and instructed to "Write about [their] day." No further instructions for length or content were given. Entries were returned to the laboratory within 48 hours. Participants wrote down the time and day of the entry, but no procedure was used to verify the accuracy of time and date information. The average amount of time between the laboratory and home diary was 8 hours and the minimum was 6 hours. It was hypothesized that naltrexone use would be associated with continued increased disclosure in the diaries.

Analysis
Planned comparisons were used to test the hypothesis that naltrexone would significantly alter the self-reports of hypertensives, but not normotensives, in the direction of less repression and greater disclosure. These comparisons are more powerful than post hoc tests (68,69) and decrease spurious findings by reducing the total number of tests and minimizing the capitalization on chance (70). Interaction analyses were precluded by the small number of participants. Tests were performed with MMatrix custom contrasts (naltrexone vs. placebo sessions) in repeated-measures GLMs. These contrasts are more powerful than the simple averaging of sessions and accounts for between-session variation. All tests were two-tailed (p < .05).

Both laboratory interviews and home diaries were assessed using Pennebaker’s Linguistic Inquiry and Word Count (LIWC2001 (71)). Five variables were selected a priori based on their relation to disclosure: self-references, positive emotion, negative emotion, insight, and somatic references. The LIWC program contains a database of words under each category and computes a ratio of target words over total words. Because ratios are used, no further controls for length of interview or narrative were used.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 MATERIALS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Potential confounding variables were first tested. Consistent with most recent research on naltrexone and mood (as measured by the POMS), there was no effect of the drug on mood for either group. Participants’ knowledge of their drug condition was tested by asking, after each session, whether they had received the drug or placebo. {chi}2 analyses showed that neither the HT ({chi} = 0.48, p = .59) nor NT ({chi} = 1.8, p = .22) group guessed their condition over chance accuracy. Alexithymia, a condition similar in appearance to repression but with a distinct etiology, was also not affected by the drug in either group (see Table 1). It should be noted, however, that alexithymia is generally considered a stable trait and much change would not generally be expected.


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  		TABLE 1. Means and Standard Deviations for Major Dependent Variables

 

Contrasts revealed a significant main effect for the drug condition on hypertensives’ reporting of life concerns (F (1,9) = 5.07, p = .046). Hypertensives disclosed significantly greater life concerns when under the active naltrexone sessions, as shown in Table 1. Life concerns reported by normotensives did not change as a function of condition (F (1,7) = 0.01, p = .944).

As measured by the Index of Self-Regulation of Emotion, hypertensives exhibited significantly less repressive coping in the drug condition (F (1,9) = 20.83, p = .004). Normotensives, however, showed no significant change (F (1,7) = 0.73, p = .427). Figure 1 presents the differential responding of hypertensives and normotensives to the drug condition.


Figure 113
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  		Figure 1. Repressive coping as measured by the Index of Self-Regulation of Emotion for hypertensives and normotensives in the drug versus placebo conditions.

 

Interview duration averaged 4.75 minutes for the normotensive group and 4.22 minutes for the hypertensive group. Analyses of interviews revealed that hypertensives used significantly more words in the drug condition as compared with the placebo condition (F (1,9) = 5.10, p = .05). The normotensive group did not exhibit a change in words between conditions (F (1,7) = 2.79, p = .15). There was no significant change in the use of self-references, positive emotion, negative emotion, insight, or somatic references (see Table 1). The content of interviews was not changed in either group as a function of drug administration. In the home diaries, HT individuals in the drug condition had tendencies for more self-references (F (1,7) = 3.17, p = .113), negative emotion words (F (1,7) = 3.64, p = .093), and insight words (F (1,7) = 4.13, p = .077) as well as a significant change in body references (F (1,7) = 6.08, p = .039). There was no tendency for the drug to affect positive emotion words (F (1,7) = 0.010, p = .923). No variables approached significance for the NT group.

Because no cardiovascular effects for opioid antagonism have been reported in previous studies, the potential effects of naltrexone on blood pressure were investigated. Systolic blood pressure was compared for high and low pressure groups across drug conditions in the baseline, interview, and recovery phases (see Table 1). The drug condition had a significant effect, increasing systolic blood pressure during interview (F (1,9) = 24.14, p = .001) and recovery (F (1,9) = 7.50, p = .02) for the hypertensive group but not for the normotensive group (F (1,7) = 0.0, p = 1.0; F (1,7) = 0.62, p = .49). Figure 2 shows the differential response by hypertensives and normotensives to the drug condition. No effects were found for diastolic blood pressure.


Figure 213
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  		Figure 2. Systolic blood pressure over baseline, interview, and recovery for hypertensives and normotensives in drug and placebo conditions.

 

Given that hypertensives exhibited both cardiovascular and cognitive changes as a result of opioid blockade, further tests were used to explore cause-and-effect relationships. Correlations between increased disclosure or decreased repression and systolic blood pressure were computed for hypertensive individuals. On naltrexone days, systolic blood pressure was significantly and positively correlated with life concerns (r = 0.822, p = .01) and negatively correlated with repression (r = –0.631, p = .05). A scatterplot of disclosure and systolic blood pressure for hypertensives in the drug condition is presented in Figure 3. In the placebo condition, systolic blood pressure was not significantly correlated with life concerns (r = 0.247, p = .49) or repression (r = –0.470, p = .24).


Figure 313
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  		Figure 3. Scatterplot of disclosure (life concerns) and systolic blood pressure in hypertensives with naltrexone.

 


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 MATERIALS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
Hypertensives exhibit a number of defensive-like traits, including less reporting of life concerns (58) and a repressive coping style (72). The present study tested one potential mechanism for this relationship: endogenous opioid activity. The opioid-peptide theory posits that a common pathophysiological pathway underlies both hypertension and the underreporting of negative states (56). Although research has shown that hypoalgesia evidenced by hypertensives is attenuated with opioid antagonism, no studies have extended this paradigm to psychological repression. The hypothesis was tested that opioid antagonism would decrease repressive coping and increase disclosure in hypertensives but not normotensives.

Naltrexone was found to increase disclosure and decrease repressive coping in hypertensives. As expected, the drug had no effect on disclosure or repressive coping in normotensives. The findings were most pronounced with the self-report measures. Although hypertensives also used 22% more words in the drug condition, there was no significant change in the number of affective target words using Pennebaker’s default LIWC dictionary. Therefore, not all tests supported the hypotheses. Significant evidence exists, however, to suggest that endogenous opioids are associated with the repressive coping evidenced by hypertensives.

Naltrexone also had a significant cardiovascular effect. Hypertensives, when exposed to the interview stressor, exhibited significantly higher systolic blood pressure with naltrexone than with placebo. This difference persisted throughout the recovery period. The normotensive group exhibited no change in response to naltrexone administration. Although no previous studies have observed a significant cardiovascular effect for naltrexone in healthy individuals, it is important to note that this is the first study to examine naltrexone use in a special population (hypertensives) under stress. These results support the opioid-peptide theory of hypertension and repression. In susceptible individuals, acute stressors may produce a large sympathetic nervous system response and subsequent increase of opioid activity. These opioids would, in turn, act on the central nervous system to diminish the experience of stress. Inhibition of this system, through opioid antagonism, removes this stress-buffering effect. Increases in systolic blood pressure observed in the present study may be the result of compensatory feedback loops activated by opioid antagonism. It is also possible that the increase of blood pressure follows heightened levels of stress experienced by the participants during opioid antagonism.

Opioids have long been implicated in the development of hypertension (48). If increased blood pressure levels can produce antinociceptive effects through endogenous opioid activity, heightened blood pressure levels may become a conditioned response (73). Some individuals may be particularly susceptible to this learned response because of a hypersensitive cardiovascular system (74), hypersensitive baroreceptors (75), or hypersensitive analgesic systems (76). If hypertension is a learned response to stressful situation, individuals exhibiting greater variability in any of these systems would be more likely to experience hypertension. It would also be important for an environment to provide sufficient stressors for such learning to occur (77). Frequent exposure to stressors (i.e., high-stress environments) may trigger more responses, leading, over time, to a sustained hypertensive condition. This hypothesis of learned hypertension is supported by research showing that blood pressure can be operantly conditioned in nonhuman primates (78,79).

Post hoc analyses showed a significant correlation between systolic blood pressure and disclosure, but only in the naltrexone condition. These analyses show that cardiovascular effects of the drug cannot be separated from psychological effects. It might be argued that the increased cardiovascular activity was a result of the increased stress of greater disclosure. Disclosure, increased by opioid antagonism, might lead to a more dystonic and stressful state, which would in turn increase blood pressure. In the interview phase, however, blood pressure was significantly greater, although no increases in disclosure were detected. Although we used a popular method for rating disclosure, it is possible that the interview and analysis protocol failed to capture a meaningful element of disclosure. It is also important to note that blood pressure increase is a symptom of opioid antagonist-induced withdrawal in dependent subjects (80).

Hypertension, often considered a "symptomless" condition, may be associated with intrapersonal and interpersonal pathology. One of these consequences may be the minimization of negative events and experiences. This altered basis of negative stimulus appraisal (10,33) could have profound effects on interpersonal relationships, because hypertensives would be less able to detect negative emotive cues in others (34). The inability to recognize the significance of conflict could lead to a failure to properly rectify conflict in close relationships (81,82). The diminished disclosure evidenced by hypertensives may also have implications for psychotherapy. Many therapists maintain that self-disclosure is vital to psychotherapy (83), but it evokes immediate feelings of vulnerability (84). Attenuated disclosure in repressive copers (85,86) and hypertensives (5,6,58,87) may make therapy difficult because the inability or unwillingness to disclose has been cited as an obstacle to therapy (88). Naltrexone is not, however, a likely treatment option for repression as a result of the drug’s hypertensive effects, interactions with alcohol, possible mood effects, and potential liver toxicity.

Although the hypotheses were supported in the present experiment, a number of factors may have weakened the power of the design. First, because healthy college students were used, clinical levels of repression were not observed. Second, the small sample size prevented the use of interaction statistics and minimized generalizability. Third, when complex cognitive styles and coping mechanisms are involved, it is unlikely that a one-time administration can cause significant change. Therefore, more significant changes in cognitive style may result only after prolonged exposure to the drug. Fourth, interpretation of the results may be limited by the use of males in the present study because recent evidence suggests gender differences in analgesic response (see (89) for a review). Fifth, portions of the study, in particular the home diaries, suffered from low response rates and weak statistical power. Therefore, interpretations of these preliminary results should be made cautiously. Future studies should make use of a larger and more diverse sample and use more sophisticated means for measuring cognitive change. Longer duration of drug conditions and ambulatory blood pressure monitoring may provide additional helpful information on this phenomenon.

The results of the present study provide preliminary support for the hypothesis that repression and hypertension share a common pathophysiological mechanism. We conclude that the actions of opioid peptides extend well beyond analgesia, and are associated with hypertension (90) and perhaps other physiological and psychological phenomena.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 MATERIALS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 
Address correspondence and reprint requests Jarred W. Younger, PhD, Stanford University School of Medicine, Department of Anesthesia, Pain Research, MC 5747, 780 Welch Rd., Suite 208. Palo Alto, CA 94304. E-mail: jyounger{at}stanford.edu

Received for publication August 5, 2005; revision received May 17, 2006.

DOI:10.1097/01.psy.0000234029.38245.c9


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 MATERIALS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

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