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Cerebrospinal Fluid and Behavioral Changes After Methyltestosterone Administration Preliminary Findings

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Cerebrospinal Fluid and Behavioral Changes After Methyltestosterone Administration Preliminary Findings ORIGINAL ARTICLE Cerebrospinal Fluid and Behavioral Changes After Methyltestosterone Administration Preliminary Findings Robert C. Daly, MB, MRCPsych, MPH; Tung-Ping Su, MD; Peter J. Schmidt, MD; David Pickar, MD; Dennis L. Murphy, MD; David R. Rubinow, MD Background: Anabolic androgen steroid abuse is asso- 104.7±31.3 vs 86.9±23.6 pmol/mL; P,.01). No signifi- ciated with multiple psychiatric symptoms and is a sig- cant MT-related changes were observed in CSF levels of nificant public health problem. The biological mecha- corticotropin, norepinephrine, cortisol, arginine vaso- nisms underlying behavioral symptom development are pressin, prolactin, corticotropin-releasing hormone, poorly understood. b-endorphin, and somatotropin release–inhibiting fac- tor. Changes in CSF 5-HIAA significantly correlated Subjects and Methods: We examined levels of mono- with increases in “activation” symptoms (energy, sexual amine metabolites, neurohormones, and neuropeptides arousal, and diminished sleep) (r=0.55; P=.02). No sig- in the cerebrospinal fluid (CSF) of 17 healthy men, at nificant correlation was observed between changes in baseline and following 6 days of methyltestosterone (MT) CSF and plasma MT, CSF MHPG, and behavioral symp- administration (3 days of 40 mg/d, then 3 days of 240 toms. mg/d). Subjects received MT or placebo in a fixed se- quence, with neither subjects nor raters aware of the or- Conclusions: Short-term anabolic androgenic steroid use der. Potential relationships were examined between CSF affects brain neurochemistry, increasing CSF 5-HIAA and measures, CSF MT levels, and behavioral changes mea- decreasing MHPG. Changes in 5-HIAA levels caused by sured on a visual analog scale. anabolic androgenic steroids are related to the behav- ioral changes we observed. In this small sample, we did Results: Following MT administration, levels of not observe a significant relationship between behav- 3-methoxy-4-hydroxyphenylglycol (MHPG) were sig- ioral measures and either dose of MT or CSF and plasma nificantly lower (mean±SD, 103.8±47 vs 122.0±50.7 levels of MT. pmol/mL; P,.01), and 5-hydroxyindoleacetic acid (5-HIAA) levels were significantly higher (mean±SD, Arch Gen Psychiatry. 2001;58:172-177 NABOLIC ANDROGENIC ste- tems in the observed effects of AAS. For roid (AAS) abuse poses a example, in rodents these steroids pro- significant public health duce brain region–specific increases in problem and has been as- b-endorphin7 and vasopressin,8 up- sociated with a range of regulate glucorticoid receptor immuno- psychiatric symptoms, including psycho- reactivity in the hippocampus,9 and bind A1 2 sis, irritability and aggression, and ma- the benzodiazepine binding site of the jor mood syndromes.3 In a previous study g-aminobutyric acid type A receptor10; fur- 4 From the Behavioral of normal men, we demonstrated that ther, AAS-induced aggression can be Endocrinology Branch even short-term administration of the AAS modulated by manipulation of central se- 11,12 (Drs Daly, Schmidt, and methyltestosterone (MT) produced sig- rotonin function. In human beings, AAS Rubinow), the Experimental nificant mood and behavioral symptoms. administration may be accompanied by in- Therapeutics Branch Two subsequent blind, placebo-con- creases in plasma homovanillic acid (Dr Pickar), and the trolled studies5,6 confirmed the ability of (HVA). In addition, steroid abuse may be Laboratory of Clinical Sciences such steroids to induce mood and behav- associated with hypomania, depression, (Dr Murphy), National ioral symptoms in both normal volun- and a dependent pattern of use.5,13 Previ- Institute of Mental Health, teers and AAS users. The mechanisms un- ous studies examining cerebrospinal fluid Bethesda, Md; and the Division of Psychiatry, National derlying the development of AAS- (CSF) have yielded valuable information Yang-Ming University, and the induced psychiatric symptoms remain about the pathophysiology of such con- Department of Psychiatry, largely undetermined. ditions, including the potential roles of so- Veteran’s General Hospital, Studies in animals and humans have matotropin release–inhibiting factor Taipei, Taiwan (Dr Su). implicated several neurochemical sys- (SRIF)14 and corticotropin-releasing hor- (REPRINTED) ARCH GEN PSYCHIATRY/ VOL 58, FEB 2001 WWW.ARCHGENPSYCHIATRY.COM 172 ©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 SUBJECTS AND METHODS procedure, subjects fasted for at least 9 hours and had had continuous bed rest for a minimum of 1 hour, except for get- ting up once to void. Lumbar punctures were conducted be- Subject selection and protocol are as previously described4 tween 9 AM and 10:30 AM on the final mornings of the base- and are summarized as follows. Twenty-three medication- line and high-dose phases. They were performed in the L4-5 free, healthy men between the ages of 18 and 42 years were interspace with the patient in the lateral decubitus position, recruited through advertisements in the hospital newslet- using a sterile technique. Seventeen of the 20 subjects un- ter of the National Institutes of Health Clinical Center in derwent successful CSF sampling in both phases. From each Bethesda, Md. Three volunteers were excluded because of subject, 21 mL of CSF were collected. The first 3 mL were medical problems or a positive drug screen. The remaining used for standard clinical studies, and the next 18 mL were 20 subjects had no significant history of psychiatric illness drawn in 3 aliquots (12 mL, 3 mL, 3 mL). The first aliquot or AAS use and were free of any recent (past 2 years) his- was subdivided into 1-mL subaliquots; the samples were tory of alcohol or substance abuse. This was confirmed with placed on ice and stored at −70°C until assayed. The follow- a standardized psychiatric interview17 administered by a psy- ing CSF assays were performed: 3-methoxy-4-hydroxy- chiatrist. After the subjects received a complete description phenylglycol (MHPG), 5-hydroxyindoleacetic acid (5- of the study, written informed consent was obtained. The HIAA), HVA, norepinephrine, dopamine, b-endorphin, protocol was approved by the National Institute of Mental prolactin, adrenocorticotropic hormone (ACTH), cortisol, Health (NIMH) Institutional Review Board (Bethesda, Md). CRH, SRIF, and arginine vasopressin (AVP). Cerebrospinal Following a 2-day acclimatization period at an NIMH fluid measures and serum MT level assays were also per- inpatient unit, all subjects received MT or placebo admin- formed on samples obtained during the high-dose phase. istered as 3 capsules, 3 times daily. These capsules were given in a fixed sequence with neither subjects nor raters aware BEHAVIORAL MEASURES of the order of administration. The following schedule was used for each subject: 3 days of placebo (baseline phase), 3 Visual analog scale ratings were completed 3 times per day days of MT (low-dose phase; 40 mg/d), 3 days of MT (high- (10 AM, 6 PM, and 10 PM) for a range of subjective behavioral dose phase; 240 mg/d), and 3 more days of placebo (with- measures. The reliability and validity of such analog scales drawal phase). Subjects were informed that the purpose of in rating subjective feelings has been established.18 The high- the study was to understand possible behavioral reactions est rating recorded each day was selected and then averaged to AAS and were told that they would be asked questions for the 3 days of that particular phase (ie, baseline or high- regarding their mood and thinking on a daily basis. dose phase). The use of highest daily rating scores was cho- sen for several reasons. The low doses of AAS used in this CSF MEASURES study (compared with doses abused) gave rise to relatively modest mood changes. Additionally, mood symptoms All subjects adhered to a low-monoamine diet beginning 2 days before the first lumbar puncture. Before the Continued on next page mone (CRH) in affective disorders15 and of endorphins 20.5±24.0 nmol/L). After MT administration, there was in addiction.16 a significant increase (compared with baseline) in CSF In an effort to further identify possible mecha- levels of 5-HIAA (t16=3.3, P=.005) (Figure 1) and a sig- nisms underlying observed behavioral changes, we per- nificant decrease in MHPG levels (t16=3.0, P=.009) formed CSF sampling in our previously described group4 (Figure 2). After the Bonferroni adjustment, P values at baseline and following 6 days of MT administration. for changes in CSF 5-HIAA and MHPG remained sig- A variety of CSF measures were obtained, including amine nificant or near significant at P#.05 and P#.1, respec- metabolites that reflect the activity of neural systems pre- tively. Other CSF measures did not change significantly sumed to underlie affect and behavioral regulation, and between the baseline and high-dose phases (Table 2). neuropeptides and neurohormones that can cause be- Changes in CSF 5-HIAA were not significantly corre- havioral disorders related to stress and addiction. lated with changes in CSF MHPG (r=0.21, P=.40). Two questions were posed in the investigation. First, Changes in CSF 5-HIAA were significantly correlated with during MT administration, are there alterations in CSF changes in activation cluster scores (r=0.55, P=.02) metabolites that have been observed to change either in (Figure 3); changes in aggressiveness (r=−0.30, P=.21) animal studies of AAS effects or in clinical syndromes in and cognitive (r=0.18, P=.49) cluster scores did not cor- humans (such as hypomania or aggression) that may be relate significantly with changes in CSF 5-HIAA. Changes associated with AAS use? Second, are such metabolic in MHPG did not significantly correlate with activation changes (if any) correlated with the observed behav- (r=−0.09, P=.72), aggressiveness (r=0.03, P=.91), or cog- ioral changes following AAS use? nitive (r=0.31, P=.22) cluster score changes.
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