The prevalence of LDL receptors estimated by Nobel Prize winners, Goldstein and Brown, was risky. We can see however that the new numbers provided by the Regeneron study supported Goldstein and Brown’s estimate. This should be pretty big news.
Imagine when Einstein’s theory demanded that light from a particular star would not travel in a straight line because of the Sun’s gravity. It was pointed out that this bending of light could be proven during a solar eclipse. This event presented an enormous risk for Einstein’s theory and reputation. When the time came, the light behaved precisely as Einstein’s theory said it would, and to his well-deserved acclaim.
Imagine however that his theory had not been so famous. Imagine a culture that did not respect the scientific record. Imagine that someone else renamed the whole event and altered its interpretation of the theory in his own favor. Now imagine the same event takes place, supporting Einstein’s daring idea, but because culture has been retaught a different language, and a redefined set of terms, Einstein’s prediction is considered obsolete and even incorrect — precisely when events actually lend it the strongest support to date.
This is pretty much what is happening with the Nobel Prize winners’ definition of FH and their prevalence estimate. The verification of their estimate should have been big news. But it wasn’t. Precisely when their numbers were supported by new evidence, their numbers were said to be wrong — by that same evidence.
Now the two Nobel Prize winners are on Regeneron’s board.
Using linguistic conflation to claim that the same, old data is somehow different, updated data
Recent publications are using linguistic conflation to claim and “prove” that Goldstein and Brown’s original estimate is mere “dogma.”
In the above presentation at the FH Foundation — whose topic was the history of FH prevalence — the original 1:500 was said to be from a “Joe Goldstein.” There was no mention of him as Joseph Goldstein, Nobel Prize winner — and co-discoverer of the LDL receptor. The entire backdrop to the presentation is more or less: the old dogma has fallen to new examinations and discoveries.
And this is pretty much the refrain of countless new studies of FH prevalence: “The established rate is X-number, but new studies show Y-number.” As if 1:500 was a former belief, overthrown by new evidence. But has the old FH-as-LDLR estimate really changed within epidemiological discipline? It is very clear that when the constituents of the new prevalence studies are broken down that the numbers match up pretty well with the Nobel Winners’ estimates.
Mismanagement of the scientific record spanning separate publications is, for whatever reason, partly to blame. Through a series of scientific papers, instead of pursuing specifics and maintaining a parallel perspective with their targets of criticism, specifics are dropped …. and this allows a “conclusion drift” toward generalization and a blending of names. Different populations are added to a single name, and this aggregation is presented as if an “increase” over one of its constituents. Once our research chases down all the terms, this “epidemiology” is as much of a truism as it is to say that the whole pie is bigger than one of its slices.