> for cvd risk mortality if you exclude the largest single study that also had a long duration (WHI 2006) it made CVD risk mortality significant, so one of thos

> for cvd risk mortality if you exclude the largest single study that also had a long duration (WHI 2006) it made CVD risk mortality significant, so one of those long duration studies is dragging the results the opposite way. Right, and the proposed pathway by which SFA increases CVD risk is via increases in ApoB/LDL-c. What LDL-c differences did they achieve in WHI 2006? Additionally, the substitution is important. DGs recommend replacing SFA with PUFA, whereas in WHI the intervention group largely replaced SFA with CHO. Interestingly, the control group had higher levels of PUFA and MUFA, which may also explain the paltry change in serum cholesterol. If you want to claim that 15 more incidents per 1000 of a disease that is one of the top killers in the western world is a rounding error, then go for it. I don’t think that’s a reasonable position, personally. As for the speculation about higher levels being healthy - speculate away, but I don’t see why anyone should believe it’s the case when a) it runs contrary to the body of evidence on the subject b) there’s no actual evidence backing up that speculation.