Aromatase inhibitors give women more muscle mass

Anastrozole ~ Men show little change in body composition if you block their estradiol production with the enzyme aromatase. [Clin Endocrinol (Oxf). 2008 Jun 25. [Epub ahead of print].] In women things are different, oncologists at the University of Pittsburgh in the US discovered. Aromatase inhibitors boost muscle mass in the fair sex.

Let’s start with a recap: there are two sorts of anti-oestrogens. First of all there are SERMs, like tamoxifen and clomiphene. These block the estradiol receptors and thus prevent estradiol from doing its work. They often actually take over some of the functions of estradiol. In men SERMS raise testosterone levels; in women they don’t.

And then there are the aromatase inhibitors like anastrozole [structural formula shown above]. These interfere with the functioning of the enzyme aromatase as a result of which less androstenedione and testosterone are converted into estradiol.

Chemical athletes use anti-oestrogens to counteract the side effects of some anabolic steroids, but also to restore the body’s own testosterone production after taking a course of steroids. Doctors subscribe the same anti-oestrogens for breast cancer survivors, as they reduce the chance of the cancer returning.

Tamoxifen ~ Doctors have collected a lot of information on the side effects of SERMS, in particular those of tamoxifen. Long-term use of tamoxifen [structural formula on the right] leads to negative changes in body composition. Women often lose muscle mass and build up fat.

Not much is yet known about the side effects of aromatase inhibitors.

Letrozole ~ For example, what is the effect of aromatase inhibitors on women’s body composition? This is the question that the researchers set out to answer in the small study they did of 82 women, who they monitored over a period of two years.

The women were all cancer survivors. Half of them were given a SERM – usually tamoxifen, but sometimes also toremifene or fulvestrant [no-AIs]. The other half were given an aromatase inhibitor, such as letrozole [structural formula shown here], anastrazole or exemestane [AIs].

During the 24 months that the study lasted the fat mass of the women who took SERMs increased by a kilogram, while there was no increase in fat mass in those who took an aromatase inhibitor.

SERMs had no effect on lean body mass, while the aromatase inhibitors led to more than a kilogram increase in lean body mass.



The aromatase inhibitors increased the amount of testosterone in the blood, and the researchers think that this was the reason for the increase in the women’s lean body mass.

Exemestane ~ We, the nit-picking compilers of this web magazine, have a teeny problem with this study: the researchers do not reveal how many of the women in the AI group were given exemestane [structural formula on the right]. Moreover, we wonder whether the miraculous effects of the aromatase inhibitors would still be observed if the exemestane had been excluded from the study.

Exemestane is not just an aromatase inhibitor: it’s also an androgen with an anabolic effect and it is an anabolic steroid.

Increased risk of non-fatal myocardial infarction following testosterone therapy prescription in men.



An association between testosterone therapy (TT) and cardiovascular disease has been reported and TT use is increasing rapidly.


We conducted a cohort study of the risk of acute non-fatal myocardial infarction (MI) following an initial TT prescription (N = 55,593) in a large health-care database. We compared the incidence rate of MI in the 90 days following the initial prescription (post-prescription interval) with the rate in the one year prior to the initial prescription (pre-prescription interval) (post/pre). We also compared post/pre rates in a cohort of men prescribed phosphodiesterase type 5 inhibitors (PDE5I; sildenafil or tadalafil, N = 167,279), and compared TT prescription post/pre rates with the PDE5I post/pre rates, adjusting for potential confounders using doubly robust estimation.


In all subjects, the post/pre-prescription rate ratio (RR) for TT prescription was 1.36 (1.03, 1.81). In men aged 65 years and older, the RR was 2.19 (1.27, 3.77) for TT prescription and 1.15 (0.83, 1.59) for PDE5I, and the ratio of the rate ratios (RRR) for TT prescription relative to PDE5I was 1.90 (1.04, 3.49). The RR for TT prescription increased with age from 0.95 (0.54, 1.67) for men under age 55 years to 3.43 (1.54, 7.56) for those aged ? 75 years (p trend = 0.03), while no trend was seen for PDE5I (p trend = 0.18). In men under age 65 years, excess risk was confined to those with a prior history of heart disease, with RRs of 2.90 (1.49, 5.62) for TT prescription and 1.40 (0.91, 2.14) for PDE5I, and a RRR of 2.07 (1.05, 4.11).


In older men, and in younger men with pre-existing diagnosed heart disease, the risk of MI following initiation of TT prescription is substantially increased.

PMID: 24489673 [PubMed – in process] PMCID: PMC3905977

Source: http://www.ncbi.nlm.nih.gov/pubmed/24489673

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