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The Effect of 6 Months of Androgen Deprivation Therapy on Muscle and Fat Mass in Older Men With Localized Prostate Cancer

Posted on: Friday, 20 January 2006, 06:00 CST

By Boxer, R S; Kenny, A M; Dowsett, R; Taxel, P

Abstract

Objective. To evaluate body composition changes, specifically skeletal muscle mass, in men receiving androgen deprivation with luteinizing-hormone releasing hormone-agonist (LHRH-A) for prostate cancer (PCa) in comparison with healthy controls.

Design. Retrospective analysis of body composition changes in men with prostate cancer receiving LHRH-A therapy from 2 clinical trials compared to men without prostate cancer serving as a placebo- control in another clinical trial.

Setting. Clinical Research Center in Connecticut.

Participants. Thirty men (> 60 years) receiving 6 months of LHRH- A therapy for PCa were compared to a healthy group of 25 men without PCa.

Measurements. Appendicular skeletal muscle/height^sup 2^ (ASM/ ht^sup 2^), lean and fat mass were assessed by dual energy x-ray absorptiometry. Total testosterone levels were assessed by enzyme immunoassay.

Results. At baseline, 12/30 (40%) of the treatment group and 7/ 25 (28%) of the control group (p = 0.11) met criteria for sarcopenia. There were no differences between control groups in ASM/ ht^sup 2^ or lean mass. The LHRH-A group had a higher percent body fat than the control group, 29.8 6.3 versus 26.3 4.6 (p = 0.02). ASM/ht^sup 2^ and lean mass decreased in the LHRH-A group from 7.5 0.9 kg to 7.3 0.9 kg (-2.3% 0.03; p ≤ 0.001) and 53.5 5.4 kg to 52.3 5.3 kg (-2.1% 0.03; p ≤ 0.001), respectively. There was no muscle loss in the control group. At 6 months, the LHRH- A group had increased percent body fat from 29.8 6.4 to 32.2 5.8 (9.5% 0.13; p ≤ 0.001), whereas the control group had decreased in percent body fat from 26.6 4.6 to 25.3 5.0 (-3.8% 0.08; p = 0.02).

Conclusions. Men undergoing LHRH-A treatment for PCa decreased appendicular skeletal muscle and lean tissue and increased body fat within 6 months of initiation of therapy. Lifestyle changes or medical interventions to minimize the effects of androgen deprivation therapy for PCa deserve investigation.

Keywords: Sarcopenia, prostate cancer, body composition, androgen deprivation

Introduction

Prostate cancer (PCa), a disease that primarily affects men over age 60 years, is a common malignancy and cause of cancer death in US men [I]. A widely used treatment modality for PCa is luteinizing- hormone releasing hormone-agonist (LHRH-A) therapy (e.g., leuprolide and goserelin) for the establishment of medical castration [2]. In depot form, it leads to castrate levels of testosterone and estrogen (2) in 3-4 weeks [3]. Previously, this treatment was reserved for those with PCa and bony mtastases [4], but more recently it has been used for locally advanced disease without metastases, or as neoadjuvant therapy prior to radiation or seed implantation.

Sarcopenia has been denned as the unintentional loss of skeletal muscle mass and function associated with aging [5]. It is distinct from muscle atrophy and occurs in the absence of focal pathology [6]. The prevalence of sarcopenia, as denned by Baumgartner et al. [7], is approximately 25% in healthy, community-dwelling older adults and the rates increase with age [8]. Increased disability, falls and impaired function have been associated with low skeletal muscle mass in two studies of communitydwelling adults [9,10]. Further, adverse health outcomes such as hospitalization [11], worsening activity of daily living, disability [12] or mortality [12,13] were associated with poor performance on measures that rely on muscle mass such as walking speed or grip strength. Contributors to skeletal muscle mass in healthy, community-dwelling older adults include factors such as body mass index (i.e., nutrition), testosterone levels, growth factors, strength and activity [8,9].

Cross-sectional studies demonstrate individuals treated with LHRH- A have decreased lean tissue mass and increase in fat mass [14,15]. Few studies have determined the longitudinal changes in skeletal muscle mass or lean tissue mass in men with PCa treated with LHRH-A and the studies lack control groups [16,17,18]. We, therefore, evaluated the body composition, prevalence of sarcopenia and changes in skeletal muscle and fat mass in a group of men with PCa following 6 months of LHRH-A therapy compared to a group of community- dwelling men without PCa.

Methods

Study population

Control subjects were community dwelling men over the age of 60 years without the diagnosis of PCa and with PSA levels < 4.0 ng/dl. The controls were placebo participants in a 1-year randomized controlled trial of testosterone replacement in healthy older men [19]. Men from the greater Hartford area were recruited by newspaper advertisements, contacts at senior citizen centers and physician referrals. Men with chronic medical conditions such as kidney, gastrointestinal or liver disease, diseases of bone metabolism or taking medications known to cause or treat osteoporosis (other than calcium or Vitamin D supplementation) were excluded.

Community-dwelling men over age 60 years with a diagnosis of localized prostate were eligible for the study; the men were receiving treatment with LHRH-A therapy (e.g., leuprolide and goserelin) as neoadjuvant treatment prior to radiation or seed implantation. These men received evaluation during participation in one of two studies: a 6month double-blind randomized controlled trial (RCT) of bone mineral density in which subjects received either a bisphosphonate versus placebo OR a 1-year observational study of BMD during which they received 9-weeks of micronized estradiol versus placebo. Men receiving estradiol therapy were not included in this analysis. However, men receiving bisphosphonates were included since there are no known effects of bisphosphonates on muscle or fat mass. Body composition analyses were obtained on all men within 3 weeks of their first LHRH-A injection and at the end of 6 months of therapy. Men with the following conditions were excluded from the studies: subjects with PCa and bony mtastases as diagnosed by bone scan or PSA > 20 ng/ml, chronic medical conditions such as kidney, gastrointestinal or liver disease, significant coronary disease or thromboembolic disorders, diseases of bone metabolism or on medications known to cause or treat osteoporosis (other than calcium or Vitamin D supplementation).

There was no crossover of individuals between the groups, i.e., no man that had been a control was diagnosed with prostate cancer and subsequently placed in the treatment group. All subjects signed written informed consent, approved by the University of Connecticut Institutional Review Board.

Body composition/testosterone assay

Total and regional lean tissue masses of volunteers were determined from a whole body dual x-ray absorptiometry (DXA) using a DPX-IQ scanner (GE Medical Systems Lunar, Madison, WI); all scans were obtained by the same certified technician. Whole body scan provided total lean body mass (LBM (kg)), total fat mass (kg) and total body bone mineral content (kg). Appendicular skeletal muscle mass (ASM) was determined by combining the lean tissue mass of the regions of the arms and legs, excluding all other regions from analysis [2O]. We adjusted ASM for height by dividing each by height2 (m2). We used the definition of sarcopenia proposed by Baumgartner et al. [7], defined as appendicular skeletal muscle mass/ ht2 > 2 standard deviations below the sex-specific young-normal mean from a reference population (7.26 kg/m2 ). Normative levels for ASM/ height2 are taken from a previous study [7]. The coefficient of variation (CV) for ASM/height2 was 1.09%.

Statistical analysis

Baseline and clinical characteristics were reported using means and standard deviations stratified by treatment group. One-way analysis of variance (ANOVA) was used to test the difference in baseline characteristics between the treatment groups. Repeated measures analysis of variance was used to assess change in ASM/ height2, lean tissue mass, and percent fat mass over 6 months between groups. For each participant we calculated the percentage change in ASM/height2, lean tissue mass, percent fat mass from baseline to 6 months. We checked variables for normality of distribution and for the impact of outliers. All analyses were performed using SPSS version 11.0.

Results

The baseline characteristics of 30 men treated with LHRH-A for PCa and 25 healthy controls are shown in Table I. Men in the LHRH-A group were younger, mean age 71.9 + 7.1 years, than the control group, mean age 75.1 + 4.6 years (p = 0.05). At baseline, the LHRH- A group had a higher percent total body fat than the control group 29.8 + 6.3 kg versus 26.3 + 4.6 kg (p = 0.02), and 12/30 (40%) of the treatment group and 7/25 (20%) of the control group (p = 0.11) met criteria for sarcopenia. Body mass index is not different between the groups (p = 0.41).

After 6 months of LHRH-A therapy, the treatment group had a decrease in ASM/height2 from 7.5 + 0.9 kg/m^sup 2^ to 7.3 + 0.9 kg/ m^sup 2^ (time X group effect p ≤ 0.001), while the control group did not change. Total body lean tissue decreased in the LHRH- A group from 53.5 + 5.4 kg to 52.3 + 5.3 kg (time X group effect p ≤ 0.001) after 6 months of therapy, a decline of 2.3%, compared with no change in the contro\l group. Body fat increased in the LHRH-A group from 29.8 6.4% to 32.2 5.8% (time X group effect p ≤ 0.001), a change of 9.5 + 0.13 % and there was no change in body fat in the control group (Table II, Figure 1).

Discussion

We found that older men receiving LHRH-A lose skeletal muscle mass in the first 6 months of therapy, compared with no change in older communitydwelling men without PCa. ASM/height2 declined by 2.3% in men treated for 6 months with LHRH-A for localized PCa. Longitudinal data from a population-based cohort revealed that healthy men lose only 0.8% ASM over a 2-year period and provides a comparison to the large changes seen in those receiving ADT [21]. Low ASM is associated with decreased physical activity and disability [7,22,23] and suggests that investigations of interventions to prevent the loss of skeletal muscle associated with LHRH-A treatment are warranted.

Other cross-sectional and uncontrolled longitudinal studies have similarly found changes in body composition with androgen deprivation therapy. Declines in lean body mass of 2.4-5.0% and increases in body fat of 9.4-14% have been reported [16,18,24,25]. A controlled cross-sectional study found higher body fat in men who received ADT compared with men who had PCa but did not receive ADT and healthy aged-matched controls, but found no differences in lean body mass [15].

The cause of the muscle loss with LHRH-A therapy is not known. The loss could be due to changes in testosterone levels. Our previous work suggests that higher basal testosterone levels are related to higher ASM/height2 in both men and women [8,26]. Young men with hypogonadism treated with testosterone replacement therapy increase muscle mass and fat-free mass [27]. Bhasin et al. have established the dose-response relationship between testosterone and muscle mass in young men. They found that young men (age 18-35 years) first treated with LHRH-A and then replaced with 5 doses of testosterone ranging from subphysiologic (25 mg weekly) to supraphysiologic (600 mg weekly) resulted in a graded dose- dependent increase in testosterone levels and improvement in muscle mass at testosterone levels of approximately 500 ng/dl or greater [28].

Table I. Baseline characteristics.

Table II. Body composition of LHRH-A treatment group versus control group at baseline and six months.

Another potential contributor to muscle loss with LHRH-A treatment may be decreased activity due to fatigue, side effects, and/or quality of life [29,30]. Men with early PCa treated with hormone suppression reported significantly more difficulty with physical function, fatigue and quality of life than men receiving no treatment or local therapy [29]. Stone et al. reported more fatigue, both mental and physical, diminished strength endurance and quality of life, but no change in reported functional abilities following androgen deprivation therapy [3O]. The effect that increased fatigue and/or decreased quality of life has on diminished activity and de- conditioning leading to skeletal muscle loss has not been evaluated.

Figure 1. Percent change in LHRH-A versus control group from baseline to 6 months.

In addition to diminished skeletal muscle mass, lower extremity and upper body strength have been reported to decline with androgen deprivation therapy [25,15,30]. Few trials have addressed interventions to counter the functional loss associated with LHRH-A therapy, although one trial showed improvement in upper and lower body strength following resistance exercise training in men receiving androgen deprivation therapy for curative or palliative treatment for PCa, compared to a decline in muscle strength in a non- intervention control group [31].

Interestingly, we have found that men with PCa have higher total body fat mass at baseline compared with healthy controls, despite similar values for BMI. This finding has not been previously reported. Our groups are not comparable at baseline for both body fat and age, but increased age is associated with higher fat mass [32], making the findings even more striking. A number of observational and epidemiologic studies have found an association between obesity and PCa risk [33-37] based on BMI and anthropomorphic measurements of body fat. Measurement of adipose and lean tissue mass is more accurate by DXA than anthropomorphic measurements such as skin fold testing [38]. In a cross-sectional study, Basaria et al. [15] evaluated men with PCa on LHRH-A versus men with PCa not receiving LHRH-A and compared each of those groups to age-matched controls (n 20 per group). In contrast to our report and epidemiological data, they found no difference in DXA total body fat mass between untreated men with PCa and age-matched controls. The mean percentage body fat mass in their group of men with PCa not receiving LHRH-A was 26.2%, very similar to our control group without PCa, although the mean age of their group was younger than ours (66 compared with 75 years, respectively). An Italian study compared body composition by DXA in 11 men with PCa (prior to LHRH- A) with 11 age- and BMI-matched controls and found that lean body mass was significantly lower at baseline in men with PCa than the controls. They found no differences in fat mass [39]. In a cross- sectional study that measured body composition by DXA, Stoch et al. found that men receiving LHRH-A treatment had higher fat mass than those with PCa not receiving this therapy; however, they did not have body composition data on a control group [40]. Thus, the data is inconclusive regarding the relationship between fat mass and risk of PCa.

The study has several limitations. Information on physical activity or quality of life is not available on the men with prostate cancer so we cannot address whether changes in physical activity or quality of life contributed to their body composition changes. The control group, a placebo arm for a testosterone intervention study, did not change physical activity or health related quality of life in the observation period [19,41]. Further, testosterone levels are only available on a subgroup of the men with prostate cancer so analysis was not performed. If baseline testosterone levels are lower in the control group, then changes we found in body composition between the groups would be conservative.

Conclusion

We found that older men receiving LHRH-A lost 2.3% of skeletal muscle mass in the first 6 months of therapy and demonstrated a 9.5% increase in body fat. These changes are significantly more than those seen in a control group of men without PCa. The cause of these changes is unknown, but most likely results from the loss of testosterone and may also be impacted by increased fatigue and decreased quality of life associated with androgen deprivation therapy. In addition, we found that untreated men with PCa had a higher percent body fat than controls, which is consistent with epidemiological data. However, this observation requires further study.

Acknowledgements

Study concept and design: Drs Boxer, Kenny and Taxel. Acquisition of subjects and data: Drs Kenny, Dowsett and Taxel. Analysis and interpretation of data: Drs Boxer, Kenny and Taxel. Preparation of manuscript: Drs Boxer, Kenny, Dowsett and Taxel.

Sponsor's role: This work has been supported by the Patrick and Catherine Donaghue Research Foundation, General Clinical Research Center (MO1-RR06192), Claude Pepper OAIC (5P60AG13631) and a grant from Aventis/Proctor and Gamble. Dr Kenny has been supported by fellowships from the Brookdale Foundation and the Paul Beeson Faculty Scholar Program. None of the sponsors were involved in design, methods, subject recruitment, data collection or analysis and preparation of this paper. In addition, we wish to thank Linda Gregory, Pamela Fall and Alison Kleppinger for assistance with completion of the work.

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R. S. BOXER1, A. M. KENNY1, R. DOWSETT3, & P. TAXEL1,2

1Center on Aging, 2Department of Endocrinology (PT), and 3Radiation Oncology (RD), University of Connecticut Health Center, Farmington, Connecticut, USA

Correspondence: A. Kenny, Center on Aging, MC-5215, University of Connecticut Health Center, Farmington, CT 06030-5215, USA. Tel: +1 860 679 3956. Fax: +1 860 679 1307. E-mail: kenny@uchc.edu

Copyright CRC Press Sep-Dec 2005

Source: Aging Male

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