Unfortunately there is no approved oral medicine to lower Lp(a) that I am aware of. (I mean given a normal LDL.) Statins don't lower it afaik. An oral medicine named muvalaplin is being tested for it.

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brandonb 5 days ago | parent | next [-]

There's a clinical trial for a new drug, lepodisiran, which lowered Lp(a) by 93.9%.

Outside of that, if your Lp(a) is high, then the first strategy would be to choose a lower ApoB target than you would otherwise. (Every Lp(a) particle is also an ApoB/cholesterol particle, but 6x more atherogenic. So by lowering ApoB, you are compensating for the effect of high Lp(a))

Summary of the current research/evidence is here: https://www.empirical.health/blog/lipoprotein-a-blood-test/#...

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throwaway7783 6 days ago | parent | prev | next [-]

There are some in trials. I'm part of one by Eli Lily. Lp(a) sucks, is genetic and so far there was no medication.

	▲	dr_ 5 days ago \| parent [-]
		The best way to get tested may be in conjunction with a trial. This was can potentially enroll.

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agensaequivocum 5 days ago | parent | prev | next [-]

This guy talks about lowering his own with collagen and vitamin C

https://x.com/gregmushen/status/1917780163242385586

And another guy lowering his with Amla, lysine and vitamin C

https://x.com/gregmushen/status/1924660722786828584

	▲	OutOfHere 5 days ago \| parent [-]
		It is nonsense because I have truly taken all four in good daily doses for years, and my value is still high.

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d4704 5 days ago | parent | prev | next [-]

I’ve read that (injection currently, not oral) ‘PCSK9 inhibitors’ may help lower Lp(a) where few other things do today.

https://my.clevelandclinic.org/health/drugs/22550-pcsk9-inhi...

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anonnon 5 days ago | parent | prev [-]

Oddly enough, there's evidence that saturated fat intake inversely affects Lp(a) levels: https://pmc.ncbi.nlm.nih.gov/articles/PMC10447465/

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OutOfHere 5 days ago | parent [-]

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

	▲	anonnon 5 days ago \| parent [-]
		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.