Someone asked me the other day how to inhibit myostatin. In case you don't know, myostatin is the body's way of slowing down muscle growth. The more myostatin you produce, the less muscle you grow. The less myostatin you have, or the more you inhibit it, the more muscle you gain. Animals with genetic myostatin deficiencies are ridiculously proportioned slabs of pure muscle, like the double-muscled cattle or the bulley whippet. And so people are often trying to figure out new ways to block myostatin in the body. One new way is via gene therapy that increases production of follistatin—one of the main inhibitors of myostatin in the body. Follistatin binds to myostatin and makes it less active, opening up the potential for greater muscle growth.

While that's certainly interesting, I don't think you need to go that route right away.

Raw fertile eggs were one of the classic bodybuilding foods. Bodybuilding legend Vince Gironda said that eating 36 fertile eggs a day was comparable to using Dianabol (a steroid). There may be something to it; as it turns out, fertile eggs actually contain follistatin. There are several studies showing that fertile eggs can actually downregulate myostatin. 

Vitamin D also increases follistatin and decreases myostatin. This is one reason why vitamin D supplements can actually counteract sarcopenia (muscle wasting), and it's why I advocate training with weights outside in the sun. Sun and steel are incredibly synergistic—and follistatin increase/myostatin inhibition might be one reason why.

Cruciferous vegetables like broccoli may be able to inhibit myostatin via follistatin. The responsible compound appears to be sulforaphane, which is richest in broccoli sprouts. I gotta say: I'm a big broccoli guy. Always have been.

Finally, creatine will help. Research shows that taking creatine in concert with resistance training has a noticeable effect on myostatin levels. I maintain that creatine should be in everyone's supplement stack. It's not even really a supplement, but rather an important nutrient.

I don't think any one of these interventions will have as powerful an effect as follistatin gene therapy or having a genetic myostatin deficiency, but taken together they may exert a noticeable effect. How about you, folks? Are you doing anything to reduce myostatin or increase follistatin?