While it happens naturally in cows and some breeds of whippets, myostatin mutation is an extremely rare condition in humans. The first case was documented in 2004 with a German boy, born in 2000. At four years old, the boy had muscles twice the size of other kids his age, and half the body fat. He could hold sevenpound weights with his arms extended. DNA testing showed he had a myostatin mutation. Liam Hoekstra was diagnosed with the same gene mutation in 2008 as a toddler. He, too, was exceptionally strong, with 40 percent more muscle mass and almost no body fat. Both boys produce little or no functional myostatin. At the same time, researchers at the Mayo Clinic found that exceptionally frail elderly women have the highest levels of myostatin.
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After the Johns Hopkins scientists reversed age-related muscle loss in mice using a short-term myostatin inhibitor, there were high hopes this would be a cure for sarcopenia, muscular dystrophy and other muscle-wasting conditions.
THE UNDIAGNOSED EPIDEMIC
Sarcopenia has been described as the undiagnosed epidemic. Both the Center of Disease Control (CDC) and the EU put in in their top five worldwide health risks. Yet the medical profession is still deciding if sarcopenia is a disease, a syndrome or simply a side effect of aging. Since there isn’t a general consensus, it remains hard to diagnose. Muscle quality and functional abilities also play a key role in a diagnosis, along with the amount of muscle loss. Estimates are that 10–20 percent of people between the ages of 60 to 70, and 50 percent of those over 70, are suffering from the condition. Add to that thousands of younger people already exhibiting pre-sarcopenia (thanks to our couch-potato lifestyle) and this could easily turn into an epidemic. Initial results were enough to pique the interest of the pharmaceutical companies. Around 2005, they started investing heavily in myostatin inhibitors. However, myostatin remains a mystery. In 2013, the pharmaceutical companies Acceleron and Shire shelved their ACE-031 myostatin inhibitor. Results in the first test group were promising: 48 healthy women aged from 45–75 were each given a single injection of ACE-031, based on their body weight. Their lean-body mass was boosted and a 3-mg/kg dose saw an increase in muscle volume of five percent. It wasn’t long before generic copies of ACE-031 cropped up in gyms across North America as a magic bullet for weightlifters and bodybuilders. Unfortunately, the results were short-lived, and ACE-031 presented some disturbing side effects. The original test group began experiencing a sudden and unexplained drop in FSH (follicle-stimulating hormone), which is related to the functions of ovaries and fertility. A test group of kids with muscular dystrophy developed nosebleeds, bleeding gums and dilated blood vessels. While not life-threatening, the reactions were serious enough for ACE-031 to be pulled. Stamulumab (MYO-029), developed by Wyeth Pharmaceuticals (now owned by Pfizer), was also pulled after disappointing results from the Phase 2 trials. Both compounds continue to be peddled in bodybuilding circles, despite their obvious lack of efficacy.
HIKE THE ALL NEW REBEL FUSION CREW Moisture control from the inside-out
The buzz on myostatin remains strong enough that the World Anti-Doping Agency has put any type of myostatin inhibitor (working or not) on their banned-substances list. Think of the Olympic records that could be shattered with athletes carrying 40 percent more muscle than their competitors. We may still see a myostatin cure for muscle wasting. Pfizer continues to invest in myostatin research. Should Johns Hopkins get their current ACVR2B compound to work (and to market), Pfizer will be sharing the profits with them. For now, turning back time and stopping muscles from ageing remains an elusive promise. Diet and exercise remain our best tools in the fight to stay strong and healthy. adventuramag.ca fall 2014 29