The prevalence of FH is 1/500, not 1/200.
The difference between FH as 1/500 and FH as 1/200 is entirely linguistic … it is a product of equivocation. What follows is a study — not of science — but of equivocation masquerading as science.
A promise to my reader: With a little time, the eyes will adjust to
the dark obscurantism behind FH identification procedures and the gimmicks will be rendered obvious … simple.
Click here to begin a detailed, historical narrative. I present examples, screenshots, and references. I also have introductory videos immediately below. Scroll down further for reports in PDF (large).
Part 1(a) here: Introductory video to the FH language strategy.
Part 1(b) here: 2 examples of “fact-ectomy” and “citation kiting.”
Part 2: The FH Patient Swap.
- Overview of Parts 1 and 2
- Part 1: After the restoration of citation, linguistic and mathematical integrity the prevalence of Familial Hypercholesterolemia (FH) is 1 in 500. It is not “twice” former estimates, unless we replace epidemiology with linguistics.
- Part 2: Those identified with the “scoring systems” (DLCN, etc.) are mostly different people from those identified through genetic testing. This has serious consequences.
- Longer Video (22 min) outlining the history and manipulation of FH prevalence estimates and diagnostic procedure:
“Citation Kiting, Obscurantism and Trafficking Humans in FH Literature (Familial Hypercholesterolemia)”
After reconciling the Danish reports (see below), I explored the larger picture. In this later report, I first present a history of FH prevelance, which turned out to be a history of linguistic manipulation. Then I demonstrate the undeniability of the FH Patient swap. (See videos Part 1a and 1b above for a simplified presentation.)
Download PDF (86 pages, 20 MB)
“Reconciliation of the Danish and Regeneron FH reports”
This is where I began my research. Two reports from Denmark, by the same four authors and using the same population study, conclude comparable prevalence estimates. However, under deductive analysis, the two studies identify mostly different people. I also detail other shenanigans that I found in these reports along the way. (See video Part 2 above for a simplified presentation.)
Download PDF (139 pages, 20 MB)
“How Citation Kiting uses FH to misdiagnose FCH, METS, T2DM and the Obese“
This is my last work on FH. Consider it an “evidentiary exhibit” with analysis. I provide original screenshots of material with analysis commentary. We show how FH researchers pursued accuracy and precision up to around the year 2000, but then through “citation kiting,” diverted FH “results” toward inaccuracy and indefinability.
Download PDF (60 pages, 31.6 MB)
Note: There are two forms of FH, the
heterozygous and the homozygous. The heterozygous inherited the problem from
only one parent, and the homozygous from both parents. The heterozygous FH
(HeFH) have a prevalence of 1 in 500. The homozygous (HoFH) have a prevalence
of 1 in 1,000,000. Because this is a genetic disease there is a mathematical relationship
between these two prevalence numbers. So
when HeFH prevalence doubles, it also increases the estimate for HoFH prevalence — and of course it goes the
other way around too.
 How do authors in the FH industry calculate from the HeFH to the HoFH? Although calculation of HoFH from the HeFH, begins with “2pq” of the Hardy-Weinberg equation and one does not know the exact value of “q,” because “p” (or the prevalence of HoFH) is so extreme, the value of “q” will always be so close to 1 that, practically speaking, it is inconsequential when resolving “2pq.”