Mitt Romney was clearly primed for the inevitable question about human embryonic stem-cell research. So when it was his turn in Thursday's debate among Republican presidential hopefuls, he pounced like a grad student taking his orals. MSNBC's Chris Matthews said that "Mrs. Reagan wants to expand federal funding of embryonic stem-cell research. Will that progress under your administration?" To which Romney replied, "It certainly will. Altered nuclear transfer, I think, is perhaps the best course." Matthews apparently had no idea what he was talking about--he seemed to think it was a form of adult stem-cell research, since he fired back, "embryonic; embryonic"--but Romney was ready: "Altered nuclear transfer creates embryolike cells that can be used for stem-cell research. In my view, that's the most promising source."

Leaving aside the "most promising" part, Romney got the science right. Altered nuclear transfer is the latest darling of those in the pro-life camp who have decided that "pro-life" might strike a discordant note if it means that people suffering from Parkinson's disease, spinal-cord injury and other diseases and conditions that might be treated with embryonic stem cells or with drugs derived from stem-cell research are left to suffer and die. By "latest," however, we mean at least two years old. It was in the spring of 2005 that bioethicist William Hurlbut of Stanford University made the case for "Altered Nuclear Transfer as a Morally Acceptable Means for the Procurement of Human Embryonic Stem Cells" in a paper in the academic journal Perspectives in Biology and Medicine; he laid out the same case before the President's Council on Bioethics in December 2004. What makes this technique "morally acceptable" to Hurlbut and others who believe that human life begins at conception and that the 16-cell blastocyst is a human being is that the ball of cells you create in the lab can never develop into a fetus.

If you are a 45-year old woman who weighs 140 pounds and stands 5 feet, 9 inches tall (in other words, several layer cakes away from obesity), with a blood pressure of 130/80, then you have a 70 percent greater risk of having a heart attack than if your blood pressure were below 120/70. If you are a 50-year-old man who weighs 180 pounds and stands 6 feet tall, with a blood pressure of 160/90, then your risk of heart attack is 130 percent greater--that is, 2.3 times as much--than if your blood pressure and weight were lower.

I mention these facts (you can calculate your own risk of heart attack, heart failure and stroke based on your sex, weight and blood pressure at the American Heart Association's nifty site) because of two new studies on genetic factors that raise the risk of heart disease. Two competing teams of researchers writing in the online issue of the journal Science both found a genetic variant that raises the risk of heart disease 15 to 20 percent in people who carry one copy of it (that is, they inherited the variant form mom or dad, but not both) and 50 percent in those who carry two copies of it (both mom's egg and dad's sperm carried the variant). The variant lies on chromosome 9. Neither team knows what exactly it does. They've ruled out the possibility that it acts through mechanisms known to raise the risk of heart disease, such as increasing blood pressure or bad cholesterol, but promoting atherosclerosis remains a possibility.

Just to emphasize those numbers: factors we already know about raise the risk of heart attack significantly more than these (still mysterious) new heart-risk genes. So why the fuss?