In 2011, Dr Daniel Donner began a 5-year project to investigate an anabolic steroid originally designed for cattle and its potentially therapeutic effects in treating obesity, diabetes and heart disease, particularly in aging men with low testosterone.
In 2015, the journal Endocrinology published a peer-reviewed scientific article by Dr Daniel Donner et al., titled “Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome“.
The paper describes a possible direction of treatments for a recently characterised disease now known as Testosterone-deficient Metabolic Syndrome (TDMetS). Those most susceptible to this disorder are middle-aged to late-aged men (40-50+ years) who develop any of the following symptoms/diseases:
- low libido and/or erectile dysfunction associated with low testosterone levels,
- lean mass (muscle) loss,
- abdominal obesity, and/or
Over previous decades, testosterone has been more rapidly prescribed to men as they pass 40 years of age. Generally patients considered for testosterone replacement therapy (TRT) are those who report to suffer any symptom of sexual dysfunction which may or may not then be followed up by a blood test to measure testosterone levels. Clearly, this wasn’t the most robust system. Following recent developments to our understanding of the body as we get a little softer around the edges, we now know that replacing low testosterone with testosterone may not actually have the intended effect in overweight individuals. Fortunately, recent restrictions to the prescription of testosterone have since been implemented while researchers have gotten to work on the issue.
Briefly, the body of an aged and overweight man is a complex environment, particularly in terms of how it manages, produces and converts many hormones. Most interestingly perhaps are the findings of recent research in the field concluding that all the extra fat tissue that sits around our waist is far from dormant – in fact it’s actually more like a gland or organ all of its own accord.
We now know that the fat cells or ‘adipocytes’ that replicate and grow to excess in obese individuals, actively convert circulating testosterone (the male sex hormone) to estrogen (the female sex hormone). Additionally, we know that the more estrogen we produce (by converting testosterone to estrogen in adipocytes) the louder the signal to the brain to stop its communication with the testicles to produce testosterone. Another mechanism which works against men as they grow to be overweight, is the fact that incremental progression towards obesity i.e. by slow and steady development of insulin resistance over time, directly inhibits the testicular production of testosterone as well.
To make matters trickier, it’s important to understand that testosterone is quite a critical hormone in telling the new (stem) cells produced by the human body to become muscle or bone. Without adequate levels of testosterone, these new stem cells are more likely to become fat cells and contribute to a person becoming overweight or obese.
So, growing overweight mechanistically slows testosterone production, and lower testosterone mechanistically increases weight gain. That’s a vicious physiological cycle!
In response to this somewhat messy problem faced by more and more men in our rapidly aging global population, the paper by Dr Daniel Donner et al., explored the effects of traditional treatment with testosterone in obese rats with low testosterone.
As expected by the researchers, the testosterone didn’t really do what many prescribing doctors might have hoped for. The testosterone treatment being used to treat these obese, low testosterone rats was essentially being turned into estrogen by all the fat surrounding these not-so-little research subjects.
To prove the point further, the researchers took a special ‘designer’ steroid originally intended for use in cattle which, unlike testosterone, cannot be converted to estrogen by fat cells.
The treatments with this designer steroid were far more successful at reducing obesity, restoring muscle mass and improving metabolic function than the traditional testosterone.
As promising as these findings are, further research into these designer steroids in human trials is critical to assessing their safety. The main point of this study was to dig deeper than previous studies and confirm or refute the complexity of the Testosterone-deficient Metabolic Syndrome, with a view to developing better treatments for men with this condition.
On an exciting note, many designer steroids (also called Selective Androgen Receptor Modulators, or ‘SARMs’) are currently being evaluated in clinical trials for potential treatment of humans in the not-too-distant future.