OK, I won’t go in to HOW I got to this point, it’s one of those “Connections” things… (started with an Autistic Veterinarian named Temple Grandin)
But I ended up at the Belgian Blue.
They deliberately shave the fur to show off the muscles on these cows and bulls. And do it in places only a chef could appreciate… Now that’s a “rump roast” if ever I’ve seen one.
Here is a short video about them that touches on the genetics involved:
So what is so interesting about a cow?
These cows have LOADS of muscles.
The growers and developers are interested in that, as it gives more pounds of saleable meat per animal. All well and good. What interested me was another directions. These animals are the result of a standard breeding program to select for a ‘knockout gene’. There is a gene that controls the growth of muscles. These animals have a broken copy…
Belgian Blue cattle are a beef breed from Belgium, known in French as Race de la Moyenne et Haute Belgique. Alternative names include Belgian Blue-White, Belgian White and Blue Pied, Belgian White Blue, Blue and Blue Belgian. The sculpted, heavily muscled appearance is known as “double muscling”, and is a trait shared by the Piedmontese breed. They are named for their typically blue-grey mottled hair colour, although it can vary from white to black.
The Belgian Blue has a natural mutation of the gene that codes for myostatin, a protein that counteracts muscle growth. The truncated myostatin is unable to function in this capacity, resulting in accelerated lean muscle growth, due primarily to hyperplasia rather than hypertrophy. The defect in the breed’s myostatin gene is maintained through linebreeding. This mutation also interferes with fat deposition, resulting in very lean meat. The neonatal calf is so large that Caesarean sections are routinely done. Double-muscled cows also can experience dystocia, even when bred to normal beef bulls or dairy bulls, because of narrowing of the birth canal.
Knockout the gene, instant Mr. Atlas … at least in cows and bulls. But all mammals are far more alike than different at the genetic level. Especially at the level of basic control genes and structural genes. It is almost 100.00% probable that we have the same gene in us.
So, first person to invent / discover a way to bind to the gene, bind to the protein it produces, or otherwise make a drug that slows down or shuts off that gene is going to be a $Billionaire. Take a pill until your muscles are the size you like, then cut back… Want an army of Super Soldiers? A pill a day is all it takes, no need for all those weights and running… (though the initial form would likely be a shot instead of a pill).
We already have drugs that work by these methods on other genes and other proteins. This cow tells us exactly what gene to hit. The rest is just lab work and “perspiration” (followed by 10 years at the FDA for America and endless carping from all sorts of folks…)
Yes, you would need to initially “sell” it as medicine for folks with various forms of wastage. The Elderly, cancer patients, and several other diseases. But we all know it would not stay there for long. There would likely be a big secondary market on farms raising other breeds of cattle, sheep, pigs, you name it.
I doubt if anyone else has “made that connection” just yet, but it’s only a matter of time…
So, who wants to be a millionaire overnight, (a billionaire a bit later)? All I ask is that you call it The Smith Treatment, and put a picture of a well muscled Blacksmith on the package ;-)
Update, just moments later
So I did a bit more digging… Looks like there is almost the same drug / idea in the works. It hits several other pathways too, so could likely be improved to be more selective, but it DOES increase muscle mass.
Follistatin is being studied for its role in regulation of muscle growth in mice, as an antagonist to myostatin (also known as GDF-8, a TGF superfamily member) which inhibits excessive muscle growth. Lee & McPherron demonstrated that inhibition of GDF-8, either by genetic elimination (knockout mice) or by increasing the amount of follistatin, resulted in greatly increased muscle mass. In 2009, research with macaque monkeys demonstrated that regulating follistatin via gene therapy also resulted in muscle growth and increases in strength. This research paves the way for human clinical trials, which are hoped to begin in the summer of 2010 on Inclusion body myositis.
It’s going to get a whole lot more interesting around here in a few more years…
More on other species with the gene already identified including some individual humans here:
In 2004, a German boy was diagnosed with a mutation in both copies of the myostatin-producing gene, making him considerably stronger than his peers. His mother, a former sprinter, has a mutation in one copy of the gene.
An American boy born in 2005 (Liam Hoekstra) was diagnosed with a clinically similar condition but with a somewhat different cause: his body produces a normal level of functional myostatin, but because he is stronger and more muscular than most others his age, his doctor believes that a defect in his myostatin receptors prevents his muscle cells from responding normally when exposed to myostatin.