As reported in USA Today and a host of other news sources: Taking their cue from nature, researchers have developed the first treatment shown to dramatically shrink the fatty plaques that clog arteries, a study reports Wednesday.
The experimental drug is a synthetic version of a protein discovered in a handful of Italian villagers who had healthy arteries and lived long lives despite having low levels of good cholesterol, called HDL.
In its place, the 40 villagers have a different form of HDL, a protein dubbed ApoA-1 Milano. The new research shows that a genetically engineered version of the protein reversed the progression of coronary artery disease, says lead researcher Steven Nissen of the Cleveland Clinic.
“The concept is sort of liquid Drano for the coronary arteries,” said Nissen, a cardiologist.
Five infusions of ApoA-1 over six weeks reduced plaque deposits by an average of 4%, 10 times the reduction seen after years of taking cholesterol-lowering statin drugs. The benefit was even more pronounced in the large, inflamed plaque-filled bulges that are prone to burst and cause heart attacks, reducing them by as much as 34%.
“I almost fell out of my chair when I saw what happened,” Nissen says.
Although the study was small, involving just 47 patients with severe heart disease, the results were so dramatic that researchers say it heralds the start of a new offensive against heart disease. Currently, researchers concentrate on drugs that lower levels of bad cholesterol (LDL), which carries fats into arteries. In the future, researchers will try bolstering HDL, which hauls fats away.
The treatment must be given intravenously, so it’s likely to be used in people who have had heart attacks, says the study in The Journal of the American Medical Association.
“The ApoA-1 story is remarkable, beginning with discovery of rare individuals in a small Italian town and leading to the development of a potential new therapy,” Daniel Rader of the University of Pennsylvania says in an accompanying editorial.
Esperion, the biotech firm that makes the protein, is planning a much larger trial involving 1,500 to 2,000 patients, prior to seeking government approval to market ApoA-1. Government approval is probably a decade away.
Seriously. As for the study on the genetic composition of the few Italians that seem to tolerate cholesterol well, how do the researchers know if the gene is on its way in or out, or if it is even a mutation at all? Maybe the rest of us are the mutants, and they’re “originals.” Ever thought of that?
There’s practically no doubt whatsoever that the people in this Italian village are the mutants in this case. The fact that they were in an isolated village with very little population influx that also had Catholic Church marriage records going back for centuries was the key to being able to determine the textbook passing-down of a new gene from generation to generation. The people in the village who have the Apo gene all have this one particular couple as their great-great-great-etc. grandparents; everybody else in the village doesn’t. It’s textbook Mendelinan inheritance.
In a broader sense, we are all mutants. The DNA in our sex cells is constantly being modified by chemical mutagens like mercury and natural radiation sources like cosmic rays and many other reasons. The children who spring from these modified sex cells are literally all mutants but most of the time the effects of having a single modified gene is either invisible or tragically visible as some form of birth defect. The Apo is like a genetic winning lottery ticket – it is the rare instance where something good comes of the mutation. Evolution is based on the accumulation of such rare good mutations over generations and is the primary reason sex is worth all the trouble it causes in our lives.
Finally, thanks for your comment, “…tolerate cholesterol well…” because it shows a misconception on your part that trying to rectify uncovered a hazy area in my own area of understanding as well which I’ve since thought through. People don’t just “tolerate” cholesterol as something that only shows up uninvited in their bodies from stuff they eat. It is actually a hormone that is manufactured by the human body and is used as a building block in the manufacture of other hormones, such as testosterone. The way it gets into our food is that the animals we eat manufacture it for use in their bodies, and we tend to eat the parts of their bodies where their cholesterol concentrates, which throws off the balance of cholesterol we make for ourselves. That’s why I made my comment about French Fries, which are high in cholesterol only because they are cooked in animal fats high in cholesterol. There’s no reason why the gene for this new “mutant” cholesterol couldn’t be inserted into a genetically engineered potato. Fries made from such a potato would then contain cholesterol from two sources – the cooking fat (bad) and the inserted gene (good). Then our fixation with eating French fries could provide us all with a daily supply of this Apo-based cholesterol that would singlehandedly end heart disease in America. Pass the catsup.
Mr. James:
As for your response linking Mendel’s patterns of inheritance to mutations, I would suggest that textbook Mendelian inheritance is more a matter of recessive and dominate genes, and the role of mutations in this case appears to be marginal.
Why do I think it to be true, and quite the opposite of what you’ve implied? Firstly, the stability or recoverability, of the species system in question relies on information being retained, not tossed out. For instance, how does one go about proving that a favorable arrangement of genes was at one time “new” information, without simultaneously disproving the very genetic principles that have kept the genes ‘in the family’ for all these generations? “Blending”, you see, was part of the original Darwinian hypothesis. And the fact that ancestors with the gene which breaks down cholesterol didn’t produce an “intermediate form”, representing both the parent carrying the gene and the parent who did not, shows exactly why Mendelian genetics is a better approach for a systematic biology over Darwinian evolution. Iow–they are not even the same thing.
All such things considered, if we all do happen to be mutants, (as you’ve implied) and no one person is not a mutant, then how does one disprove said hypothesis? There’s just no means for a falsification mechanism if ALL members of this community, and we, are mutants.
regards..