The Story of Follistatin

The story of follistatin really began in 1807 (although inadvertently) with the discovery of a breed of cattle in Belgium that had excessive amounts of lean muscle tissue in conjunction with minimal levels of body fat.

As such, this breed underwent linebreeding until this excess muscle became a “standard” feature amongst their kind – we know this breed today as the Belgian “blue cow.”

Though we didn’t know it at the time, this was actually the first discovered case of myostatin deficiency.

For many years (almost 200 in fact) nothing of note took place in regards to the development or understanding of follistatin – discovering, highlighting the effects of and understanding the myostatin molecule were to be the breakthrough elements we needed to fully appreciate precisely what follistatin was and how it functioned.

This discovery was to take even longer – not occurring until 1997.

Though we had seen its effects in action (or its lack of effect) as displayed by the “blue cow”- we were simply none the wiser in regards to precisely what myostatin was.

Our discovery of this “muscular” cow breed didn’t do a great deal in terms of making sense of the ominous substance; we simply found these creatures to be “novel” and an excellent commercial opportunity to exploit without really ever penetrating beneath the surface to discover precisely why they were born in such a manner.

It wasn’t until 1987 that we finally “discovered” and isolated follistatin via the discovery of the FST gene; labelling it as an “FSH” suppressing protein or as it was soon abbreviated (roughly during the same time frame) “follistatin” – It was discovered in the follicular fluid of porcine ovaries.

This discovery preceded the discovery of myostatin by a decade, and ultimately paved the way for the follistatin “situation” we now find ourselves in today in regards to the research we are performing.

Following the aforementioned discovery of myostatin in 1997 – we were able to piece together the jigsaw that told the story of the interaction between follistatin and myostatin, and how the two form an almost “yin and yang” type relationship to promote hormonal homeostasis in regards to muscular hypertrophy (growth.)

A further breakthrough discovery came in 2004 when Schuelke and colleagues documented a case of extreme myostatin deficiency occurring in a human infant.

This case allowed us to fully appreciate precisely what physiological changes can occur in a human when myostatin presence within the system is negated.

Furthermore, we found ourselves (in 2007) with another animal specimen in the form of the now fairly infamous dog “Wendy.”

Similarly to the cattle variety previously discovered, she too was born with a severe myostatin deficiency.

Over the course of these discoveries coming to fruition during their respective years, animal testing was being performed with follistatin (some of which were the aforementioned tests on mice, the results of which were analysed in the “inhibition of myostatin” section.)

These tests yielded remarkable results in regards to precisely what follistatin may be capable of in a human host when used to suppress myostatin levels.

Theoretically, it would produce similar results to those found in the “natural” specimens above – this is what ultimately yielded the human trials we are currently performing to this day.

As you’re already well aware through reading up to this point though – conclusive evidence / results in regards to precisely how much of an effect the follistatin 344 gene / virus will have in regards to muscle growth currently remains to be seen.