Don't throw those juicy steaks away yet.
Scientists believe they may have discovered how to make the fats that are most hazardous to our hearts no more harmful than the fats that are supposed to be good for us, like fish oil. And what's even more important, the discovery may launch us on a course that could eliminate heart disease.
"If it works as well in us as it does in mice, it would push us in that direction," said Lawrence L. Rudel, leader of the research team who's a professor of comparative medicine at Wake Forest University Baptist Medical Center. Rudel admits that's a very long shot at this point, since no human clinical trials are even on the horizon, but the research, published in Arteriosclerosis, Thrombosis and Vascular Biology is tantalizing.
Rudel's team fed laboratory mice six different diets that ranged in fats from the good stuff, like olive oil and flax oil, to several types of saturated fats, the stuff that many experts believe is killing us by driving up our cholesterol and clogging our blood vessels. Half of the mice were just plain old lab rats, but the other half had been genetically altered to remove a complex protein, called the ACAT2 enzyme.
At the end of 20 weeks (a long time in the life of a mouse), the untreated rats that had dined on saturated fat were lucky to still be alive, with high cholesterol levels and evidence of atherosclerosis, or clogging of the blood vessels.
But the mice that had the enzymes removed were doing great.
"They are so healthy and look so good it makes you ask why we even have it [the enzyme]," Rudel said. That includes mice that were fed stuff that even fast food joints would reject.
Or as the researchers formal report notes, "Regardless of the diet fed, the mice [without the enzyme] were protected from atherosclerosis."
And here's a surprise. The mice that consumed all that deadly fat didn't get any fatter than the ones that were fed fish oil and other polyunsaturated fats, the so-called good fats.
"They are normal weight," Rudel said, and they showed no side effects from the treatment.
That all sounds too good to be true, and maybe it is. What works for mice frequently doesn't work for humans, although we are amazingly similar genetically. So the next step is to try the same procedure in monkeys. That test should take a couple of years. And then, if the Food and Drug Administration approves, human clinical trials could begin.
But first, a couple of problems need to be resolved. The mice had to be injected with a compound that inhibits the enzyme's actions, and Rudel doesn't believe frequent injections to control cholesterol would appeal to many people. So he's working with a large pharmaceutical company to see if it's possible to achieve the same results with a pill.
"The company that makes those compounds would very much like to go there," he said. "I don't know how fast they can get there, but that's certainly high on their agenda."
The target of the research is an enzyme that modifies cholesterol. There are hundreds of different types of enzymes in the human body, produced in living cells to cause or accelerate chemical reactions in other substances. This particular enzyme was previously implicated in the rise of the so-called bad cholesterol, LDL. So it was a natural target for Rudel's team.