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It doesn't help if LDL gets raised due to the SFAs, as LDL is an independent risk factor.


I was just noting the oddness of Lp(a) responding inversely to SFA intake (the reverse of LDL), which also contradicts the conventional wisdom that Lp(a) isn't amenable to lifestyle interventions.

You could theoretically increase SFA to target Lp(a) while still using lipid-altering drugs to target LDL.




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