1/ These are the words of Michel de Logeril, French Cardiologist with no COI, on FH: The argument put forward by cholesterol propagandists is that HeFH patients are suffering from exactly the same disease as HoFH patients, but less severely,
2/ and should benefit from the same treatments. From a marketing point of view, the argument is massive: as heterozygous cases far outnumber homozygous cases, the treatment of both can only be profitable ! However, there is no serious scientific argument to corroborate this.
3/ In fact, this total absence of scientific data is rather surprising. However, there is no serious scientific argument to corroborate this. In fact, this total absence of scientific data is rather surprising. HoFH cases are highly specific. These patients sometimes,
4/ but not always, have exceptionally high lipoprotein blood levels, and fatty deposits around skin, eyes, cardiac valves, atrial wall. These incongruous cardiac locations, only observed in HoFH, probably explain the occurrence of early CVD, sometimes before puberty, and
5/ these are certainly not juvenile atherosclerotic plaques, there is no such thing. Among the patients bearing the genetic traits susceptible of generating high concentrations of lipoproteins, and I speak here exclusively of Heterozygous cases - some also bear genetic traits
6/ that promote clotting, and therefore increase the risk of thrombosis, and consequently the risk of MI or CVA. This has been very well documented scientifically in HeFH patients. HoFH cases are too rare for this type of study to be undertaken.
7/ In the absence of a protective lifestyle, HeFH patients may of course suffer CV complications, but these are more due to their clotting anomalies, than their cholesterol level. These clotting anomalies are generally not taken into account by cholesterol experts 😀
8/ They remain undiagnosed and un-treated. When doctors encounter raised cholesterol levels in familial hyperlipoproteinemia patients, they nearly always attribute CV complications to cholesterol levels, when the true culprits are the patients' lifestyles, their inherited
9/ clotting anomalies, and high thrombosis risk. Statins are unlikely to influence the risk attached to these patients' clotting anomaly and, unless they adopt a more protective lifestyle, they will relapse. When they do survive, doctors raise their statin dose with the best
10/ of intentions but without seeing that it completely fails to provide their patients with any added protection. Most FH patients do not respond well to statin therapy, and the new injectable antibodies are not a success either. They are based on illusions and misleading
11/ propaganda. Let us just have a re-think before placing FH patients into the hands of the sorcerer's apprentice.
