Thanks for the link to the guidance document; it isn't exactly a fun read but I got through the majority of the bits that seemed relevant. Having read the guidance I didn't feel convinced that the evidence was sufficiently strong for someone with "normal" cholesterol levels to risk the side effects (documented in spacedoc.com, gpnotebook and elsewhere), especially as the reported beneficial mechanism for this group seems not to be fully understood.
Maybe this is a case of a (very) little knowledge being a dangerous thing, but ... I was confused by a couple of statements in the GPnotebook guidance: "It is hypothesised that there are two types of atherosclerotic lesions: atherotic (soft, lipid rich, there is often inflammation which destabilises the plaque's fibrous cap, the risk of plaque rupture makes these dangerous) and sclerotic (hard, collagen-rich, these are safe). The statin family of drugs alters the characteristics of the lipid core and reduces inflammation. The fibrous cap is stabilised preventing rupture. The total volume of the plaque may remain unchanged." Yet it also says: "... however, no statistically significant differences were seen for cardiovascular mortality or stroke". Elsewhere I've read that a rupturing atherosclerotic lesion can lead to stroke so if the hypothesis about statins stabilising the lesion is correct why has no significant improvement in stroke rate been seen?