This is why the conversation about removing fat from diets is so confusing. There is more than one type of saturated fat. Chain length of the molecule matters. Replacing animal derived sat fat with poly or mono unsaturated fats (plant based) has been shown to be protective, but most saturated fat is replaced with refined carbs (in other words with sugar and grains not fruits and vegetables). Grains are carbs, but not all carbs are grains, despite what reading the low carb blogosphere would suggest.
Mean intake of SFAs accounted for 9.0-11.3% energy intake over time, and was mainly composed of lauric acid (12:0), myristic acid (14:0), palmitic acid (16:0), and stearic acid (18:0; 8.8-10.7% energy). Intake of 12:0, 14:0, 16:0 and 18:0 were highly correlated, with Spearman correlation coefficients between 0.38 and 0.93 (all P<0.001). Comparing the highest to the lowest groups of individual SFA intakes, hazard ratios of coronary heart disease were 1.07 (95% confidence interval 0.99 to 1.15; Ptrend=0.05) for 12:0, 1.13 (1.05 to 1.22; Ptrend<0.001) for 14:0, 1.18 (1.09 to 1.27; Ptrend<0.001) for 16:0, 1.18 (1.09 to 1.28; Ptrend<0.001) for 18:0, and 1.18 (1.09 to 1.28; Ptrend<0.001) for all four SFAs combined (12:0-18:0), after multivariate adjustment of lifestyle factors and total energy intake. Hazard ratios of coronary heart disease for isocaloric replacement of 1% energy from 12:0-18:0 were 0.92 (95% confidence interval 0.89 to 0.96; P<0.001) for polyunsaturated fat, 0.95 (0.90 to 1.01; P=0.08) for monounsaturated fat, 0.94 (0.91 to 0.97; P<0.001) for whole grain carbohydrates, and 0.93 (0.89 to 0.97; P=0.001) for plant proteins. For individual SFAs, the lowest risk of coronary heart disease was observed when the most abundant SFA, 16:0, was replaced. Hazard ratios of coronary heart disease for replacing 1% energy from 16:0 were 0.88 (95% confidence interval 0.81 to 0.96; P=0.002) for polyunsaturated fat, 0.92 (0.83 to 1.02; P=0.10) for monounsaturated fat, 0.90 (0.83 to 0.97; P=0.01) for whole grain carbohydrates, and 0.89 (0.82 to 0.97; P=0.01) for plant proteins.
Here is a skeptical view.
Evolocumab is an antibody just like the weapons used by the immune system to fight infection.However, it has been designed to target a protein in the liver with the name PCSK9.
And ultimately it makes the organ better at whipping bad cholesterol out of the blood and breaking it down.
Other trials have shown such antibodies have cut bad cholesterol levels by 60% and Amgen is not the only company looking at this approach.
Cranky Scottish doctor Malcom Kendrick offers an even more skeptical view. Kendrick doesn't think that cholesterol causes cardio-vascular disease (CVD) so a drug that lowers cholesterol will not lower CVD. Kendrick also notes that Pfizer abruptly ended its PCSK9 inhibitor development.
We can't afford PCSK9 inhibitors at their current price. By we, I mean either individuals or our healthcare system. If our model of healthcare is pay for value, 1% to 2% reductions in nonfatal events are worth something. But they are not worth many thousands of dollars per year. And no, we don't need a complex modeling study to tell us the cost of this drug will have to come down.
There are many reasons to dump a project and cut your losses, of course, but it does charge the imagination with speculation of possible answer.
Pulling the plug when 27,000 patients had been fully enrolled. What on earth did they see. Something more than slightly worrying. I guess we will never really know, but that is one hell of a write off.