someone else online summarized the genetics part as the following:
Mandelian randomisation studies show that LDL-c is causative in atherogenic plaques 1 and metabolic ward RCTs show that SFA intakes increase LDL-c, while the decrease in SFAs lead to lower total and LDL-c 2.
But yes, almost all nutrition science is a bit inconclusive because of genetic variation.
Forgive me, because I’m struggling to understand the linked information, but as someone with atherosclerosis this is an issue close to my heart (ha!).
I just want to make sure I understand you.
Your link to the european heart journal says that the causal link between LDL and ASCVD is “unequivocal”.
I think the WHO study says (amongst a lot of other complicated stuff) that replacing SFAs with PUFAs and MUFAs is more favourable than replacing SFAs with complex carbohydrates? The strong implication being (although I couldn’t see this exactly) that higher SFA intake contributes to heart disease.
WHO report
someone else online summarized the genetics part as the following:
Forgive me, because I’m struggling to understand the linked information, but as someone with atherosclerosis this is an issue close to my heart (ha!).
I just want to make sure I understand you.
Your link to the european heart journal says that the causal link between LDL and ASCVD is “unequivocal”.
I think the WHO study says (amongst a lot of other complicated stuff) that replacing SFAs with PUFAs and MUFAs is more favourable than replacing SFAs with complex carbohydrates? The strong implication being (although I couldn’t see this exactly) that higher SFA intake contributes to heart disease.