Fewer than 30% of cardiologists recognized FH
  1. Regeneron’s prevalence claim is false. (So are the prevalence claims of the 1st and 2nd Danish reports.) The linguistic conflation of diverse diseases (FH +FDB +FH3 +p.Arg3558Cys as “FH”) does not increase the number of disease carriers. After we tease each constituent back out and compare them, like for like, each with its own established rate, FH-as-LDLR is not “twice” what was commonly thought, nor is FDB-as-R3500Q. And in fact FH-as-LDLR in the Regeneron report is lower than the established prevalence. Here is an analogy: If Study A declared a prevalence of 10 million horses in the world, and Study B declared a prevalence of 20 million. Study B could say, “Horses are twice as prevalent as Study A thought them to be” — unless it was revealed that Study A counted only horses, of the sort that are or can be domesticated, while Study B included zebras along with the horses, calling all of them “horses.” In one study zebras are not “horses,” while in the other study zebras are “horses.” It is deceptive to claim twice the prevalence when the only difference is in the linguistic re-definition and conflation of zebras with “horses.” To be in good faith, Study B’s focus should not be on prevalence, but on the re-definition of the target-word. Likewise, conflating FDB and FH3 with FH involves an incidental mathematical adjustment. Nothing more. Once linguistic conflation of separate diseases is understood, and the constituents itemized, the “higher prevalence” is exposed as a false claim. See slide here; full analysis click here.
  2. Whites of European descent are targeted in both Danish studies and the Regeneron-funded, USA-based study. Descendants from Central and Northern Europe have a higher prevalence of FDB-as-R3500Q than those whose ancestors are outside of these regions. Also, later pharma-funded reports cite a study from The Netherlands. (Click here.) The Netherlands has been reported to be influenced by founder effect, and likewise, the US-based Regeneron study includes a region with the highest FDB-as-R3500Q founder effect in the world. Founder effect should have invalidated both of these results. Just as we have gerrymandering in politics, we have “geno-mandering” in prevalence studies. See Slide here; full analysis click here.
  3. Inflated groups skew the results. In the 1st Danish report and in the Regeneron report, standards of diagnosis are lowered. Using the recommended clinical scoring system inflates the count with false positives. Also, in the 1st Danish report, under the table, a cutoff of 5 was used in the calculation, while “6” was printed in the text. Slide here; full analysis click here.
  4. The authors goosed the denominator of a key metric, which inflated the outcome. They also cherry-picked the most aggressive of 3 available ratios. After correcting the math and the linguistic conflation mentioned above, FH prevalence is actually lower than established estimates. See slide here; full analysis click here.
  5. The results of clinical scoring systems are inherently skewed by a selection bias. A clinical scoring system such as the Dutch Lipid Clinic Network criteria is not in itself sufficient to determine FH mutation carriers. However, it is the inherited cultural assumption, and while FH is as yet unknown, big pharma is stepping in with these angled research papers to instruct toward clinical diagnosis, while using genetic testing, not to raise the alarm of the false positives inherent in the scoring systems, but to simply sound the alarm … to get everyone moving along with their unchallenged, culturally inherited assumptions. It is this inadequacy of clinical screening that pharma needs to stay in place. Whenever the molecular/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 of those above clinical detection are not mutation carriers. The former are difficult and expensive to find; the latter, easy and profitable. Genuine FH are swapped out and false positives, swapped in. Inadequate distinction is a passageway to larger profits. It’s a publication strategy, and it’s working. See slide here; full analysis click here.

The Regeneron-funded paper further reveals the publication strategy already evident in the 1st and 2nd Danish reports. Pharma’s funding has been influencing the medical community for several years now, the results of which are off-label sales through the redefinition of what constitutes FH. Most of these patients are not HeFH LDLR carriers (nor HoFH). They are false positives, and the one’s left behind were the real carriers. The pharma-funded publications are designed to maximize profit from this misunderstanding.