(For another analysis of the patient swap see my other report: “FH Prevalence after the Restoration of Citation, Linguistic, and Mathematical Integrity.“)
Clinical scoring systems for FH, such as the DLCN, are inaccurate. If you tighten up such a system in order to avoid false positives, you leave out a majority of mutation carriers. If you loosen up the criteria to recover a number of previously overlooked mutation carriers, you bring in a disproportionately larger group of false positives. And so when the genetic proof of overlooked patients is only the message, while the recommended diagnosis is still the clinical scoring system, then those genuine mutation carriers in the academic abstract are swapped back out of consideration and real non-mutation carriers are swapped in. It’s as if a real estate developer recommended that a bulldozer operator use a map which was faulty. Now, the developer only needs to look down at his own correct map and say, “See ‘X’ marks the spot. Go!” The operator would pick up his own faulty map and act “independently,” illegally taking down a habitat and creating an empty space profitable to the developer. Likewise, Regeneron and the others fund studies which use a molecular map to show that “underdiagnosis exists!” but recommend the inaccurate map of clinical diagnosis to “get there.”
I have demonstrated this in my analysis. I reconciled two research studies, both written by the same authors, and both using the same 60,710-member population. One study focused on a genetic approach and the other was claimed to be solely a clinical scoring system. Although a similar prevalence total, they were of different populations. There was a swap of different groups when moving from one procedure to the other.
This was not a swap limited to these two papers. Whenever the genetic basis of FH is merely the message, while clinical scoring systems are recommended practice, patients are swapped. This is because the majority of mutation carriers are below clinical detection while the majority that are above clinical detection are not mutation carriers. The former are difficult and expensive to find; the latter, easy and profitable. It’s as if a Galapagos scientist made a special drug and then went out to convince everyone that there is a disease specific to a rare, sea-swimming turtle, while showing them how easy it is to find and inoculate the land-based tortoises.
 Because the two Danish studies shared the very same population I was able to work with deduction. The 1st and 2nd reports were complicated by the fact that only the four most frequent mutations were screened for. The 2nd report provides a “methodology” to complete the prevalence estimate. Reconciling these two reports therefore is quite elaborate. See this page for the mathematical proof by way of this reconciliation.
 This was not exactly true. Molecular hits were given clinical scores and thereafter considered clinical results. However, most of the results were due to clinical scoring alone. That is, although the genotypes were demoted to phenotypes, most were solely phenotypes to begin with. In parallel epistemology, this is like saying that although those with forensic DNA matches were demoted and considered equal to those with solely circumstantial evidence, most of the suspects had only circumstantial evidence to begin with.