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Whether testosterone treatment has benefits on body composition over and above caloric restriction in men is unknown. We hypothesised that testosterone treatment augments diet-induced loss of fat mass and prevents loss of muscle mass. We conducted a randomised double-blind, parallel, placebo controlled trial at a tertiary referral centre. The main outcome measures were the between-group difference in fat and lean mass by dual-energy X-ray absorptiometry, and visceral fat area computed tomography.
A total of 82 men completed the study. At study end, compared to controls, cases had greater reductions in fat mass, with a mean adjusted between-group difference MAD of —2. Although both groups lost the same lean mass following VLED cases —3. While dieting men receiving placebo lost both fat and lean mass, the weight loss with testosterone treatment was almost exclusively due to loss of body fat. The online version of this article doi: The obesity epidemic is associated with adverse health outcomes and high socioeconomic costs.
Modest weight loss provides important health benefits, but successful weight loss is difficult to achieve and maintain. Although most studies testing interventions for obesity focus on body weight, excess body fat is considered responsible for most obesity-associated health risks and associated with increased mortality independent of body mass index BMI [ 1 ]. Therefore, the benefit of energy restriction may be limited by loss of lean body mass [ 2 ]. In men, obesity is the single most important factor associated with low testosterone, overriding the effects of age and comorbidities [ 3 ].
This reduction in total testosterone levels is in part due to the obesity-associated lowering in sex hormone binding globulin SHBG. However, especially with more marked obesity, free testosterone levels are also reduced due to adiposity-associated suppression of the gonadal axis at the hypothalamic level. While the exact mechanisms are not fully understood, experimental studies in humans suggest that fat-derived adipokines and pro-inflammatory mediators may play a role in this central gonadal axis suppression [ 5 ].
In addition, preclinical evidence has shown that testosterone deficiency promotes adipose tissue accumulation but reduces myogenesis via an androgen receptor mediated pathway [ 6 ]. This bidirectional relationship between lowered testosterone and obesity is supported by clinical studies — weight loss increases testosterone proportionally to weight loss [ 7 ] and testosterone treatment reduces body fat [ 8 ].
Whether testosterone treatment augments fat loss additive to caloric restriction or prevents diet-associated loss of muscle mass is unknown. We conducted a randomised clinical trial in obese men with low to low-normal total testosterone to test the hypothesis that, following diet-induced loss of fat mass, testosterone treatment will prevent fat regain but maintain lean mass.
Each participant provided written informed consent prior to inclusion in the study. Subjects were randomly assigned in a concealed 1: The randomization sequence was generated by an independent statistician and implemented by the Austin Health clinical trials pharmacists. Participants, trial investigators and pharmacists were blinded to treatment allocation.
Trough levels represent the therapeutic target immediately prior to the next dose and are lower than steady state targets e. During weeks 9—10, subjects weaned their VLED and ordinary foods were gradually reintroduced. Subjects underwent weighing and individual counselling at every visit and were provided with written information to ensure dietary compliance. Adherence to the diet was estimated by measuring body weight at each study visit, with individualised feedback given.
The Austin Health intra-assay coefficient of variability CV was 6. Free testosterone was calculated according to Vermeulen [ 13 ]. Metabolic parameters fasting lipid profile, HbA1c, fasting glucose and c-peptide levels and safety parameters haemoglobin, haematocrit and prostate-specific antigen PSA were measured at the study hospital with assay technology used for routine clinical care as described [ 14 ].
An independent investigator reviewed week 26 safety parameters for pre-defined withdrawal criteria: Visceral fat was quantified from single axial CT images at the L intervertebral disc space using SliceOmatic version 4. Physical performance was assessed at weeks 0, 10 and 56 by four tests performed in duplicate and scored as the sum of the fastest times for each test in seconds: Other main outcome measures included change in lean mass DXA , visceral abdominal tissue CT and body weight.
Further outcome measures included anthropometric measurements, handgrip, physical function, physical activity and metabolic parameters. The power analysis for this study was based on the effect of testosterone undecanoate on fat mass reduction of 5. Given that previous studies have shown that dieting leads to loss of fat mass, we expected that the placebo group would retain some degree of fat loss by the end of the study.
Repeated measures of main outcome continuous data were analysed using linear mixed models LMEs with random intercepts to account for within-individual correlation over time. LME random effect and residual normality assumptions were checked and resulted in no noteworthy violations. An intention-to-treat analysis was also carried out where the outcome measures for study dropouts were returned to baseline.
Together with the LME analysis of the raw data, the LME return-to-baseline analysis provides protection against biases introduced due to missing data. Separate models with similar characteristics were used to assess other outcome data and safety variables. To compare repeated measurements of variables within groups between two time points, the t-test was used.
No adjustments were made for multiple comparisons on other variables. In the case of low numbers, the Fisher exact test was used. Data shown are mean standard deviation or median interquartile range , based on normality testing, using the Kolmogorov-Smirnov test with Lilliefors correction. All analyses of means were complemented with Wilcoxon non-parametric tests.
Similar results were found so the results were not reported. Analyses were conducted using R version 3. The wider variation and influence of few strong responders observed in the main outcome of fat mass, typical for obesity trials, was addressed in a sensitivity analysis using a robust mixed linear model, as implemented by the r package robustlmm [ 16 ]. This model corrects for natural heteroskedasticity and the potential influence of exceptional responders by introducing a weighing algorithm and Design Adaptive Scale estimate according to Koller [ 16 ], which is less sensitive to outliers in data than the squared error loss.
Between April and October , we assessed men for eligibility. Shown is study enrolment and follow-up. The most common reason for non-completion was failure to attend visits. By study end, trough TT increased to Luteinising hormone levels decreased from 4. At the end of the week VLED phase, both cases — At study end, cases had, compared to baseline, lost significantly more fat mass MAD —2. During weeks 10—56, loss of fat mass percentage was greater in cases than in controls MAD —2.
As the combined lean and fat mass lost in controls was similar to the amount of fat mass lost in the cases, the difference in body weight change at study end was no different between groups MAD —0.
Further, baseline fat mass did not interact with the changes in body composition. In addition, adjustment for physical activity did not alter the findings. Cases had a significant increase in handgrip strength compared to placebo 3. Both groups improved on physical performance testing but there was no difference between groups at study end. Outcomes were unchanged after imputation of missing values using an intention-to-treat analysis and return-to-baseline for missing data Additional file 1: Table S1; MAD for fat mass —3.
Similar findings were also found using non-parametric tests. Similar findings were also observed if non-completers in the placebo group were analysed separately data not shown. The major novel findings of this RCT are that, among obese men with low to low-normal testosterone submitted to a weight loss program, testosterone treatment decreased total fat mass and visceral adipose tissue, and protected against loss of total and appendicular lean mass. At the end of the initial week VLED phase, while men lost substantial amounts of weight similar to previous successful VLED studies [ 11 ], there were no differences in weight loss or body composition changes between the two groups.
At study end, there were marked differences in body composition between groups, and men receiving testosterone had greater reductions of fat mass —2. After the VLED phase, men receiving testosterone regained lean mass 3. Overall, our results indicate that, compared to men receiving placebo who lose both fat and muscle mass during diet, testosterone treatment shifts this weight loss to almost exclusive fat mass loss.
Our trial has several strengths distinguishing it from previous testosterone trials, most importantly, the successful implementation of a rigorous weight loss program and the exclusive focus on men with established obesity. By contrast, previous RCTs examining the effects of testosterone on body composition recently meta-analysed [ 8 ] were neither designed for weight loss nor had obesity as a selection criterion.
Moreover, only a few studies, not all placebo controlled, have combined testosterone treatment with lifestyle measures. A recent meta-analysis of these studies [ 17 ] suggested that testosterone treatment may have added benefits on body composition, consistent with our findings.
Compared to men completing the study, non-completers had lost less body weight and less fat mass at the end of the VLED phase of the study. Therefore, if anything, this would be expected to underestimate the benefits of testosterone treatment, especially as the drop-out rate was higher among men assigned to placebo compared to testosterone treatment.
Although it may be expected that the effects of testosterone treatment are attenuated in the context of a rigorous weight loss program, the reduction of fat mass observed here compares favourably with the 1.
This may be because we focused on obese men with a confirmed low testosterone receiving effective testosterone treatment.
This may also explain the robust increase in lean mass of 3. Testosterone treatment did not prevent the loss of lean mass during the week VLED suggesting that testosterone treatment lacks anabolic actions during acute severe caloric restriction. Testosterone treatment significantly reduced the metabolically important visceral fat even in the context of a weight loss program.
Previous RCTs of testosterone therapy, while not incorporating a weight loss program, did not find a consistent reduction in visceral fat [ 14 , 15 , 20 , 21 ], most likely because of small trial size [ 15 ], use of oral testosterone therapy [ 20 ], or less precise methodology to quantify visceral adipose tissue [ 20 ].
None of these RCTs specifically targeted obese men. Interestingly, the differences in body composition were evident despite the modest increase in endogenous testosterone levels in placebo-treated men similar to previous weight loss studies [ 22 ]. Indeed, this increase by 2. Thus, the endogenous rise in testosterone subsequent to diet appears not to be sufficient to prevent diet-associated loss of lean mass.
What are the potential mechanisms by which testosterone treatment leads to these changes in body composition? Testosterone, via androgen receptor signalling, inhibits stem cell differentiation into adipocytes and favours myogenesis [ 6 ].
Androgen receptor signalling in mature adipocytes promotes lipolysis [ 24 ] and activates anabolic pathways in myocytes [ 25 ]. The effect on fat mass may also be mediated by aromatisation to estradiol [ 26 ]. Testosterone may also have motivational effects leading to increased physical activity; in RCTs, testosterone treatment reduces fatigue and inertia [ 27 ], and androgen-deficient mice have decreased voluntary activity [ 28 ].
We advised subjects to perform at least minutes of moderate-intensity exercise each day. Subjects completed exercise questionnaires and accelerometer testing, with feedback given, to reinforce and encourage participation in exercise.
Both men receiving testosterone and placebo increased their activity during the weight loss phase.