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Mastering CanMEDS Roles in Psychiatric Residency: A Resident’s Perspective
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The Canadian Psychiatric Association Practice Profile Survey: I. Methods and General Sample Characteristics
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Switch to Mania Upon Discontinuation of Antidepressants in Patients With Mood Disorders: A Review of the Literature
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Acute Neuroendocrine Response to Sexual Stimulation in Sexual Offenders
Philip Haake, Manfred Schedlowski, Michael S Exton, Christoph Giepen, Uwe Hartmann, Michael Osterheider, Martin Flesch, Onno E Janssen, Norbert Leygraf, Tillmann HC Krüger
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Original Research

Acute Neuroendocrine Response to Sexual Stimulation in Sexual Offenders

Philip Haake, MD¹, Manfred Schedlowski, PhD², Michael S Exton, PhD¹, Christoph Giepen, MD¹, Uwe Hartmann, PhD³, Michael Osterheider, MD⁴, Martin Flesch, MD⁵, Onno E Janssen, MD⁶, Norbert Leygraf, PhD⁷, Tillmann HC Krüger, MD¹

Increasing evidence highlights the importance of neuroendocrine regulation of sexual behaviour in men (1). While dopamine agonists are stimulating (2–5), opioids suppress sexual desire and function in men (6). Plasma levels of testosterone are associated with sexual motivation (7), sexual function (8), and sexual activity (9). In addition, testosterone administration increases sexual desire of eugonadal men (10) and sexual function in eugonadal women (11).

Because neuroendocrine parameters are associated with sexual drive, they also may be linked to the development of deviant sexual behaviour on a biopsychosocial background (12,13). Indeed, positive correlations between plasma testosterone levels and violence have been reported in some studies (14–16), but not all (17). In different studies, testosterone antagonists were demonstrated to suppress sexual drive, interest, and fantasies in offenders (18–21). Further, recent trials with luteinizing hormone–releasing hormone (LHRH) agonists, which diminish serum testosterone to castration levels, significantly impaired the sexual activity of sexual offenders (22–24). Together, these studies demonstrate that chronic changes in hormonal status are able to change deviant sexual behaviour. Because these endocrine variations also change sexual behaviour in healthy men, it remains unknown whether altered neuroendocrine regulation is at least partly responsible for a high sexual drive in sexual offenders.

In a series of studies, we have recently analyzed the neuroendocrine response to sexual arousal and orgasm in healthy subjects. In these experiments, we demonstrated that plasma prolactin (PRL) concentrations increase substantially following orgasm in healthy men and women (25–30), compatible with an important role of PRL in controlling acute sexual arousal following orgasm. The suppressive effect of chronic PRL elevations on sexual activity, sexual desire, and gonadal function (31,32) supports the hypothesis that PRL may represent a peripheral regulatory factor for reproductive function or a feedback mechanism that signals central nervous system (CNS) centres controlling sexual arousal and behaviour, or both (33).

Because prolactin appears to play a regulatory role in acute sexual drive, we undertook this study to see whether sexual offenders with a high sexual drive have a different neuro- endocrine response to sexual arousal.

Subjects and Methods

Subjects
From a total of 150 inmates of the Westfalian Centre for Forensic Psychiatry, Lippstadt, Germany, we recruited 10 volunteers (mean age 38.4, SD 2.8 years). All subjects were detained because of sexual crimes. All inmate volunteers reported that they were sexually stimulated by erotic visual stimuli that showed adult women involved in sexual activity. We excluded sexual offenders with confounding physical health problems, drug or alcohol abuse, medication, or sexual dysfunctions. All subjects had an intensive, semistructured clinical interview by the consulting physician and were then preselected for high sexual drive. Sexual drive was defined by a short refractory period (< 3 minutes) and strong sexualization or a high frequency of sexual stimulation (> once daily). Because patients demonstrated tendencies to dissimulate actual sexual drive, we evaluated data from the beginning of treatment.

As an age-matched control group, we recruited 10 healthy male volunteers (mean age 38.2, SD 2.5 years) via an advertisement at the University Clinic of Essen, Germany. These volunteers underwent the same exclusion criteria as the forensic group. All control subjects were exclusively heterosexual and reported a relaxed attitude toward masturbation and pornography. Control participants reported that they had no criminal records. Volunteers of both groups were paid to participate in the study. The Ethics Committee of the University Clinic of Essen approved the study design and all experimental procedures.

Figure 1 Experimental paradigm

Experimental Paradigm
Both the forensic and the control group underwent the same experimental paradigm as previously described (25–30) (Figure 1). We requested volunteers to refrain from any kind of sexual activity and to avoid alcoholic beverages or other drugs 24 hours prior to the laboratory investigation. We implemented a balanced crossover design involving 2 sessions on consecutive days, with each session commencing at 2:00 PM. Subjects sat in a comfortable chair in front of a video screen. In the control session, volunteers viewed a neutral video (specifically, a scientific documentary about weather); the experimental session comprised 3 video sequences, each lasting 20 minutes. The first and last sections of this tape comprised a documentary about insects. The middle 20 minutes of the experimental video was an erotic film that showed exclusively adult females. We started blood sampling at the beginning of the film. We drew blood continuously at 10-minute intervals, collecting 6 samples. Following 10-minute viewing of the erotic video (the anticipatory phase), subjects in the experimental session were required to masturbate until orgasm.

Endocrine Analysis
To ensure accurate measurements and participant privacy, we employed a method of continuous blood withdrawal (25). An intravenous cannula was inserted into a brachial vein and connected to heparinized silicon tubing that passed through the test-room wall into the adjoining room. Blood was drawn with a minipump. Blood flow was adjusted to 2 ml/minute. Blood was collected into EDTA tubes that were changed every 10 minutes to allow a time kinetic of endocrine variables. Samples were centrifuged at 4EC; plasma was stored at –70EC until assayed.

PRL, follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone, and cortisol were determined by commercial assays on an automated chemiluminescence- immunoassay system (ACS 180, Bayer Diagnostics, Ludwigshafen, Germany). All samples were analyzed in duplicate. The respective intra- and interassay coefficients of variance were 2.5% and 3.6% for PRL, 2.8% and 4.6% for FSH, 4.7% and 6.3% for LH, 5.6% and 6.6% for testosterone, and 4.5% and 6.4% for cortisol.

Cardiovascular Monitoring
Heart rate and systolic and diastolic blood pressure were measured continuously in parallel with the continuous blood sampling, via a finger cuff connected to a blood-pressure monitor (Finapres, Ohmeda, Louisville).

The cables of the finger cuff also passed through the wall, with the monitor connected to a PC in the adjoining room. Cardiovascular parameters were sampled every 30 seconds, with the data averaged over the 10-minute intervals for statistical analysis and direct comparison to the 10-minute interval blood samples.

Subjective Assessment
To subjectively assess sexual arousal during the experimental session, subjects completed the Acute Sexual Experience Scale (ASES). This scale was developed to measure different qualities of appetitive, consummatory, and refractory sexual behaviour in men. It has 4 subscales with a total of 42 items. Apart from control items, the questionnaire comprises self-reporting sexual-functioning ratings using visual analog rating scales (0 to 100 mm, from “not at all” to “extremely”). The scales examine sexual functioning, both in absolute values and compared with normally experienced sexuality in a real-life situation such as masturbation and sexual intercourse. In detail, the first subscale, Appetitive Phase, assessed features of sexual arousability, lust, and desire during the first 10 minutes of erotic video presentation, when subjects remained passive. The second subscale, Consummatory Phase, evaluated the quality, intensity, and duration of orgasm and sexual release associated with orgasm during the second part of the erotic sequence. The third subscale, Refractory Phase, evaluated both negative aspects of refractoriness (such as tiredness, recovery, and soberness) and positive aspects (such as sexual release and relaxation).

Table 1  Crime committed, masturbation frequency, and ICD-10 diagnosis
Patient	Crime committed	Sexuality	Diagnosis (ICD-10)
1	Murder associated with sexual coercion	Short refractory period	F 61.0, F 65.5
2	Rape, sexual coercion	Strong sexualization	F 61.0, F 65.0
3	Exhibitionism, sexual coercion, attempted sexual coercion	Short refractory period, multiple orgasms possible	F 60.31, F 65.2, F 65.5
4	Repeated sexual abuse of children	3 orgasms in 2 hours possible	F 60.2, F 60.8
5	Grievous bodily harm, murder, attempted murder, rape, sexual coercion	Formerly masturbated several times daily	F 60.8, F 65.5
6	Sexual coercion	Formerly masturbated every day	F 60.8
7	Sexual abuse of a boy, repeated sexual coercion associated with rape and bodily harm	Formerly masturbated 3 times daily	F 60.8, F 65.9
8	Repeated rape, sexual coercion associated with bodily harm	Short refractory period (< 1 min)	F 60.2, F 66.9
9	Repeated bodily harm, repeated attempted rape, attempted murder	Formerly masturbated 2 to 3 times daily	F 60.2, F 66.2, F 65.5
10	Two murders, 1 associated with sexual coercion, sexual coercion with bodily harm	Formerly masturbated 2 to 3 times daily	F 60.1, F 65.5
aICD-10: F 60.1 Schizoid personality disorder, F 60.2  Dissocial personality disorder, F 60.31 Borderline personality disorder, F 60.8 Narcissistic personality disorder, F 61.0  Combined personality disorder, F 65.0 Fetishism, F 65.2 Exhibitionism, F 65.5 Sadomasochism, F 65.9 Disorder of sexual preference, F 66.2 Sexual relation disorder, F 66.9 General behaviour disorder related to sexual development and orientation

Additionally, all participants completed the Questionnaire for Measuring Factors of Aggression (FAF) (34). This questionnaire has 6 subscales measuring different aspects of aggression (specifically, self-aggression, reactive aggression, arousability, aggression inhibition, and openness). Further, the forensic group completed the German form of the Multiphasic Sex Inventory (MSI) (35). This questionnaire was developed to assess deviant psychosexual characteristics of adult male sexual offenders. Because it is strongly related to deviant sexual behaviour, it was not completed by the control group.

Statistical Analysis
Cardiovascular and endocrine data from all subjects were analyzed by a 3-factor repeated measures (group condition time) analysis of variance (ANOVA). If not otherwise stated, we report the group condition time interaction effect. On each scale of the ASES questionnaire, we conducted planned, paired-samples t-tests between the forensic and the control group. An alpha of 0.05 was considered statistically relevant for all analyses.

Figure 2 Subjective response to orgasm

Results

The intensive interview, together with the MSI, confirmed a high sexual drive in the forensic group, which was reflected by high masturbation frequency (Table 1). Further MSI characterization of sexual drive in this group showed that 60% scored between 4 and 14 in the Sexual Compulsion subscale, indicating an interest in sexuality ranging from “high” to “addiction-like” behaviour. We also found the forensic group to be more aggressive, as assessed by the FAF. Compared with control subjects, forensic patients rated themselves as significantly more spontaneously aggressive (mean 6.4, SD 1.4 vs mean 2.0, SD 0.84; Z[19] = –2.60, P < 0.05) and self- aggressive (mean 7.0, SD 0.8 vs mean 3.4, SD 0.85; Z[19] = –2.59, P < 0.05) (data not shown). However, the 2 groups did not differ significantly in the Openness subscale.

Figure 3 Testosterone response to orgasm

When we examined the subjective interpretation of sexual arousal and orgasm indicated via the ASES, we found that, compared with control subjects, forensic patients rated themselves significantly higher on the subscales Appetitive Phase (mean 48.8, SD 3.3 vs mean 26, SD 3.9; Z[19] = –3.25, P < 0.001), Consummatory Phase (mean 54.8, SD 3.7 vs mean 33, SD 3.3; Z[19] = –3.40, P < 0.001), and on the positive aspects of the Refractory Phase (mean 48.1, SD 4.9 vs mean 29.5, SD 4.5; Z[19] = –2.42, P < 0.05) (Figure 2). There was no between-group difference in the rating of the negative Refractory Phase.

Analysis of the cardiovascular response showed that both the forensic patients and the control subjects had comparable transient increases in systolic blood pressure, diastolic blood pressure, and heart rate during sexual arousal and orgasm (data not shown). However, sexual arousal and orgasm did not affect testosterone plasma levels in either group (Figure 3). In addition, sexual offenders did not differ from control subjects in their testosterone concentrations during either the experimental or the control sessions. By contrast, PRL levels peaked after orgasm in both sexual offenders and control subjects but remained unchanged under control conditions (F_6,108 = 13.02, P < 0.001; session ´ time interaction). However, in their response to orgasm, the groups did not differ with regard to the time or magnitude of increased PRL plasma levels (Figure 4). In addition, levels of plasma cortisol, as well as pituitary hormones such as FSH and LH, were un- affected by sexual stimulation or orgasm and did not differ between the 2 groups (data not shown).

Figure 4 Prolactin response to orgasm

Discussion

We recently demonstrated an orgasm- specific increase in PRL plasma concentrations. This suggests that PRL is a peripheral regulatory feedback mechanism controlling sexual arousal and behaviour (25–30). In sexual offenders, as in healthy men, neuroendocrine parameters have been shown to affect sexual drive, interest, and fantasy (18–24). However, whether the neuroendocrine response to acute sexual arousal, and particularly orgasm-induced PRL release, contributes to the high sexual drive observed in these patients remains unknown. Therefore, in this study we continuously monitored the neuroendocrine response of sexual offenders to acute sexual arousal and orgasm, compared with control subjects. The forensic patients reported higher sexual pleasure during exposure to sexual stimuli and during orgasm, compared with control subjects. However, sexual offenders with a high sexual drive did not differ from control subjects in their neuroendocrine response pattern, particularly in orgasm- induced PRL release.

The sexual offenders participating in this study were in- patients in a forensic hospital because they had committed sexual crimes and were carefully selected for high sexual drive combined with a short refractory period, or a high masturbation frequency, or both. These selection criteria are reflected in the subjective assessment scales: forensic patients scored high in the sexual compulsion subscale of the MSI and achieved higher scores in the ASES, compared with control subjects. Although these data clearly indicate a higher sexual drive in this forensic patient group, compared with control subjects, we cannot rule out the possibility that these differences are also partly caused by altered levels of daily sexual activity.

When we continuously analyzed cardiovascular and neuroendocrine parameters in response to sexual arousal and orgasm, we observed significant transient increases in heart rate and blood pressure in both patients and control subjects, which confirms a sympathetic activation during sexual arousal and orgasm. More important, and similar to previous observations, we observed a significant increase in PRL plasma concentrations in both groups (25–30). However, with regard to time and magnitude of the increase, sexual offenders did not differ from age-matched control subjects in their PRL response to orgasm. As well, in both forensic patients and control subjects, plasma levels of testosterone, cortisol, and the pituitary hormones LH and FSH remained unaffected by sexual arousal and orgasm, confirming earlier observations in healthy male and female subjects (25–29). Further, no significant differences were observed between forensic patients and control subjects in basal levels of all tested endocrine parameters. The forensic patients in this study did, however, score significantly higher than control subjects on the aggression scales. Since an association has been suggested between testosterone levels and aggression (14–16), higher testosterone concentrations might be expected in the sexual offender group. However, patients in this study were preselected predominantly for an increased sexual drive. In addition, the study by Bradford and McLean failed to correlate violence and aggression with testosterone concentrations (17).

Based on our previous studies and the suppressive effect of hyperprolactinemia on sexual behaviour and function, we have postulated that PRL may represent a peripheral regulatory factor for reproductive function, or a feedback mechanism that signals CNS centres controlling sexual arousal and behaviour, or both (33). The current data demonstrate that the increase in peripheral PRL concentrations following orgasm is a stable neuroendocrine response that seems to be independent of subjective sexual arousability in sexual offenders with high sexual drive. Based on the peripheral neuroendocrine parameters analyzed in this study, the data indicate that these forensic patients have mechanisms of sexual satiation similar to those of healthy men. Nevertheless, psychopharmacological treatment trials have demonstrated that the different hormones and neurotransmitters involved in the regulation of sexual behaviour of healthy men also influence sexual behaviour of sexual offenders (36,37); these include testosterone (18–24) and serotonin (38–41). It is therefore possible that, although PRL may contribute to the postorgasmic regulation of sexual desire in healthy men, its impact may be overshadowed by interplay with altered secretion of other hormones or neurotransmitters not observed in the peripheral blood.

In summary, these data demonstrate that sexual offenders with high sexual drive (as confirmed by a short refractory period or high masturbation frequency, or both, as well as by higher sexual pleasure during sexual stimulation) do not differ from control subjects in their peripheral neuroendocrine response to acute sexual arousal and orgasm; particularly, they do not differ in orgasm-induced PRL release. This study confirms that factors other than peripheral hormones influence deviant sexual behaviour. Further studies should concentrate on central neurophysiological changes in sexual offenders during sexual arousal. Until the role of biological factors in sexual crime is proven, therapy should concentrate on the patient’s psychosocial background.

Funding and Support

The work contained in this manuscript was supported by grants from the Deutsche Forschungsgemeinschaft (Sche 341/10-1 and Ja 671/1-3).

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Author(s)

Manuscript received July 2002, revised, and accepted September 2002.

1. Research Fellow, Department of Medical Psychology, University Clinic of Essen, Essen, Germany.

2. Director, Department of Medical Psychology, University Clinic of Essen, Essen, Germany.

3. Manager, Group for Clinical Psychology Department of Clinical Psychiatry, Hannover Medical School, Hannover, Germany.

4. Chief Consultant, Westfalian Centre for Forensic Psychiatry, Lippstadt, Germany.

5. Senior Registrar, Westfalian Centre for Forensic Psychiatry, Lippstadt, Germany.

6. Senior Registrar, Department of Clinical Endocrinology, University Clinic of Essen, Essen, Germany.

7. Director, Department of Forensic Psychiatry, University Clinic of Essen, Essen, Germany.

Address for Correspondence: Dr P Haake, Department of Medical Psychology, University Clinic of Essen, Hufelandstr 55, 45122 Essen, Germany

e-mail: philip.haake@web.de

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