Monkeying around with myostatin: on the road to healthier humans or human hulks?

The Hulk in Avengers The myostatin gene has been getting quite a bit of attention lately.

The buzz surrounds the idea of inhibiting myostatin either through gene therapy or via germline human genetic modification.

In this way, some hope to create people with more muscle. Myostatin, which also goes by the acronym MSTN, has an inhibitory function on muscle. Inhibit and inhibitor of muscle and you should get more muscle, right?

Data backs it up.

Animals including humans with spontaneous mutations in myostatin have unusual musculature including increases in muscle. This NEJM case report on a boy with a myostatin mutation describes a remarkable phenotype of drastically increased muscle and reduced fat. No clear pathology was associated with the condition, which is referred to as myostatin-related muscle hypertrophy. More on that condition more generally here.

Pop culture is fascinated with the idea of genetically modifying people to artificially create this kind of super-muscle condition. Would they be like superheroes? Just last week came the first report of a person, Liz Parrish, supposedly doing a DIY gene therapy to target myostatin.

Scientists have recently reported a string of super-muscled animals created through genetic modification including GM dogs and pigs.

If this kind of trend continues and increasingly involves people, what might go wrong? One possibility is that GM people who have had the myostatin pathway targeted could have other phenotypes or even diseases that we cannot anticipate.

6 thoughts on “Monkeying around with myostatin: on the road to healthier humans or human hulks?

  1. This genetic modification may infact result in unanticipated diseases. On the other hand, it can potentially mitigate reduced mobility that accompanies old age.

  2. I think that the general issue of adding bulk has been most elegantly addressed by Frank Zane:

    Recently Arnold has lent his considerable weight to the matter:

    What these two highly accomplished men have to say is not targeted towards manipulation of the myostatin gene, rather is is more fundamental. Those who would play cosmetic games by gene manipulation would do well to listen to Frank.

    I reserve my respect for a physique earned by the mindful application of effort.

  3. Paul I have already contacted Liz’s company in an effort to try experimenting with myostatin therapy. I am willing to be a human guinea pig in an effort to regain some muscle mass lost in my calf muscles in order to maintain my able to walk.

  4. ATF4, a DNA-binding factor that modulates responses to amino acid availability and ribosomal function, has been shown to be altered in both liver and fibroblasts from two strains of long-lived mice, i.e. Snell dwarf and PAPP-A knockout mice. Elevated ATF4 levels, and elevation of ATF4-dependent proteins and mRNAs, in liver of mice treated with acarbose or rapamycin, calorically restricted mice, methionine-restricted mice, and mice subjected to litter crowding extend maximum lifespan in mice. Elevation of ATF4, at least in liver, thus seems to be a shared feature of diets, drugs, genes, and developmental alterations that extend maximum lifespan in mice. However, ATF4 is a critical mediator of age-related muscle weakness and atrophy. I wonder how can interact myostatin and ATF4 in extending of lifespan.

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