> Generally, you read the papers for their methodology and their data — not for the author commentary; and then make up your own mind.

I'd say that generally it's advisable to take both into consideration given that in most cases the author of a paper likely has more domain expertise than you in that specific area. Not always, obviously, and not to the exclusion of an outside objective analysis of their data and results, but it's certainly more informative than referring someone to a page from a study with no additional context.

> that has not been funded by a pharmaceutical company

I get where you're coming from here, but it's kind of silly. And the question becomes where do you draw the line? Is a meta-analysis of a large group of studies each of which has been supported at least in part by funding from a pharmaceutical company guilty by association? That aside, the structure of research funding with regards to pharmaceuticals (at least in the US so far as I'm aware) makes the likelihood of conducting any long term, large scale study without receiving any funding from a pharmaceutical company vanishingly small. There have certainly been issues with studies funded and conducted by those companies, but that doesn't mean that all studies funded by them are instantly invalid. Nor does it mean that it's impossible to conduct a study that has received their funding without compromising its integrity. It is entirely possible to take sufficient measures to isolate those companies from the actual process and analysis of the research.

> wherein the experiment does not extrapolate from LDL values to determine mortality risk

As I made reference to earlier, I am not a subject domain expert here. That being said I did do a brief survey of the literature, reading fifteen papers published on either studies of statin efficacy or meta-analysis thereof. I may be misunderstanding what you're saying, but the studies I looked at assessed efficacy by looking at the actual number of cardiac events, strokes, et al suffered by those in the control and experimental groups. Their analysis was based on those numbers, not an extrapolation from LDL values.

> and/or shows a greater than 2% absolute reduction all-cause or CVD-only mortality risk.

Why that number? And why that number in two very different contexts? Regardless, statins have been show in numerous studies to be highly effective.

> while little more than weak associative studies have been published for secondary prevention

That's simply not true. There have been a number of large scale, long term studies on the efficacy of statins for secondary prevention and the preponderance of evidence is on the side of them being very effective.

Some of the studies I looked at:

Mega, J. L., Stitziel, N. O., Smith, J. G., Chasman, D. I., Caulfield, M. J., Devlin, J. J., … Sabatine, M. S. (2015). Genetic risk, coronary heart disease events, and the clinical benefit of statin therapy: an analysis of primary and secondary prevention trials. The Lancet, 385(9984), 2264–2271. doi:10.1016/s0140-6736(14)6173

- The primary focus of this study was looking at the efficacy of statins with relations to genetic risk profiles, but as a component of that we can see the overall efficacy of the statins across those risk profiles as well.

- "The relative risk reductions were
34% in low, 32% in intermediate, and 50% in high genetic
risk score categories in the primary prevention trials, and
3% in low, 28% in intermediate, and 47% in high genetic
risk score categories in the secondary prevention trials.
When the data were combined, the gradient of relative risk
reductions with statin therapy across low, intermediate,
and high genetic risk score categories were 13%, 29%, and
48%, respectively (p value for trend=0·0277, figure 2)."

- "With a focus on the primary prevention trials,
in JUPITER, the number needed to treat to prevent
one coronary event in 10 years was 66 for those individuals
with a low genetic risk score, 42 for those with an
intermediate score, and 25 for those with a high score. In
ASCOT, the number needed to treat to prevent one coronary
heart disease event in 10 years was 57, 47, and 20,
respectively, across the three genetic risk score categories."

MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: a randomised placebocontrolled trial. (2002). The Lancet, 360(9326), 7–22. doi:10.1016/s0140-6736(02)09327-3

- "All-cause mortality was significantly reduced (1328
[12·9%] deaths among 10 269 allocated simvastatin versus
1507 [14·7%] among 10 267 allocated placebo; p=0·0003),
due to a highly significant 18% (SE 5) proportional reduction
in the coronary death rate (587 [5·7%] vs 707 [6·9%];
p=0·0005), a marginally significant reduction in other
vascular deaths (194 [1·9%] vs 230 [2·2%]; p=0·07), and a
non-significant reduction in non-vascular deaths (547 [5·3%]
vs 570 [5·6%]; p=0·4). There were highly significant
reductions of about one-quarter in the first event rate for non-
fatal myocardial infarction or coronary death (898 [8·7%] vs
1212 [11·8%]; p<0·0001), for non-fatal or fatal stroke (444
[4·3%] vs 585 [5·7%]; p<0·0001), and for coronary or non-
coronary revascularisation (939 [9·1%] vs 1205 [11·7%];
p<0·0001). For the first occurrence of any of these major
vascular events, there was a definite 24% (SE 3; 95% CI
19–28) reduction in the event rate (2033 [19·8%] vs 2585
[25·2%] affected individuals; p<0·0001)."

Sever, P. S., Dahlöf, B., Poulter, N. R., Wedel, H., Beevers, G., Caulfield, M., … Östergren, J. (2003). Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. The Lancet, 361(9364), 1149–1158. doi:10.1016/s0140-6736(03)1294

- "The primary endpoint of non-fatal myocardial infarction,
including silent myocardial infarction, and fatal CHD was
significantly lower by 36% (hazard ratio 0·64 [95% CI
0·50–0·83], p=0·0005) in the atorvastatin group than in the
placebo group (figure 2, table 3)."

- "There were also significant reductions in four of the seven
secondary endpoints, some of which incorporated the
primary endpoint: total cardiovascular events including
revascularisation procedures (21%); total coronary events
(29%); the primary endpoint excluding silent myocardial
infarction (38%); and fatal and non-fatal stroke (27%,
figures 3 and 4). All-cause mortality was non-significantly
reduced by 13%, with non-significantly fewer
cardiovascular deaths (figures 3 and 4) and no excess of
deaths from cancer (81 assigned statin vs 87 assigned
placebo) or from other non-cardiovascular causes (111 vs
130)."

It appears that the evidence in support of the use of statins is quite overwhelming.