Not sure of the accuracy of this but its interesting to me as I have been diagnosed with FH but have no family history of premature CVD
Not sure of the accuracy of this but its interesting to me as I have been diagnosed with FH but have no family history of premature CVD
I think we all have to remember that even when we were younger many of these illnesses or conditions were either not known about or ignored. Think how young the NHS is and will not get much older if the current rabble at the top have their way. Every month of every year new things are discovered and current theories questioned and tested. This gives us a lot of information to cope with and this site is one where we try to make sense of it all together,
Well, I think a history of premature CVD is still the main reason for diagnosing FH, so I think the theory he's criticising still has a lot to tell HEART UK members, even if it's more debatable for the general population.
Also really unsure about this one "Heterozygous FH (hFH) people make a lower number of functional LDL receptors because one of their genes for this protein is naff. The other gene is fine." Other gene? One of the participants here who has had genetic screening can probably answer this: aren't there quite a few genes which might be involved? Have they even all been identified yet?
The post seems to describe treatment with combined bile sequestrant (cholestyramine) and statins, which I don't think is done any more, is it?
Anyway, a 2008 blog post from a vet about a 1980s speech about a 1970s study... there's a lot of studies since then, including the simvastatin clinical trials my father was involved in. But even so, its conclusion remains basically my current position: it appears I've got a choice between the effects of high LDL on me and the effects of statin use.
My knowledge of genetics is pretty basic, but is he referring to the fact that genes work in pairs as we inherit one chromosome from each parent. FH is autosomal dominant, so the "naff" gene as he calls it (not very nice, not mum or dad's fault) is dominant in FH overriding the unaltered gene.
My genetic test results, which I sweated blood and tears to get, tell me they have excluded 95% of the 3 main altered genes which are LDLR, Apo B and PCSK9 (exon 7). LDLR I know is on chromosome 19.
I find it difficult to get any on going information about research into FH compared to everything else I research....also not sure about him being a vet...do animals get FH? Statins for dogs anyone?