3 ms·

Ok, lets nitpick further: for cvd risk mortality if you exclude the largest single study that also had a long duration (WHI 2006) it made CVD risk mortality si

Ok, lets nitpick further: 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. We need to remember we are talking about relative risk so what does a 17% increase correspond to? 15 more incidents per 1000 participants with a ci of 24 to 2 incidents per 1000 participants among studies that were mostly moderate to high risk individuals. It's a rounding error on a low risk event that is probably an even lower risk event for most of the population. If you look at something that actually exists and is relevant you will see 100% plus changes to relative risk. All cause mortality relative risk is 2.29 in this study on the effect of smoking on women, for example: https://pmc.ncbi.nlm.nih.gov/articles/PMC6219821/ https://pmc.ncbi.nlm.nih.gov/articles/PMC6219821/ Figure six explores saturated fat cut offs and all but 2 of the events trend down for the last observation which is only at 13% energy from saturated fat, probably need to look at higher saturated fat levels to make sure the chart isn't an upside down U and we aren't stuck in the most deadly part of the curve arguing about whether we should cut more when we could increase consumption more to solve the issue. I'm sure there's more but I am out of time.

KempyKolibri 2y ago
> 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.

KempyKolibri 2y ago

> 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.